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OceanofPDF.com Gut The Inside Story of Our Bodys Most U - Giulia Enders

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For all single parents who put as much energy and love into
bringing up their children as our mother did for my sister and me.
And for Hedi.
Contents
Preface
1 GUT FEELING
How Does Pooping Work? And Why That’s an Important Question
The Gateway to the Gut
The Structure of the Gut
What We Really Eat
Allergies and Intolerances
A Few Facts About Feces
2 THE NERVOUS SYSTEM OF THE GUT
How Our Organs Transport Food
Reflux
Vomiting
Constipation
The Brain and the Gut
3 THE WORLD OF MICROBES
I Am an Ecosystem
The Immune System and Our Bacteria
The Development of the Gut Flora
The Adult Gut Population
The Role of the Gut Flora
The Bad Guys—Harmful Bacteria and Parasites
Of Cleanliness and Good Bacteria
4 UPDATE ON THE BRAIN-GUT CONNECTION
New Discoveries
Clever Cravings for Fermented Foods
Acknowledgments
References
Preface
I WAS BORN BY cesarean section and could not be breast-fed. That
makes me a perfect poster child for the intractability of the
gastrointestinal tract in the twenty-first century. If I had known more
about the gut back then, I could have placed bets on what illnesses I
would contract later in life. At first I was lactose intolerant. I never
thought about why I was suddenly able to drink milk again at the age
of five. At some point I got fat, then thin again. Then, for a long time,
I was fine—until I got “the sore.”
When I was seventeen, I developed a small sore on my right leg,
for no apparent reason. It stubbornly refused to heal, and after a
month I went to see my doctor. She didn’t really know what it was
and prescribed me some cream. Three weeks later, my entire leg
was covered in sores. Soon they spread to my other leg, my arms,
and my back. Sometimes they appeared on my face. Luckily, it was
winter at the time, and everyone thought I had cold sores and a
graze on my forehead.
No doctor was able to help me—giving me vague diagnoses of
some kind of nervous eczema. They asked me about stress and
psychological problems. Cortisone helped a little, but as soon as I
stopped using it, the sores just came back. For a whole year, in
summer and in winter, I wore tights to stop my sores from weeping
through my pants. Then I pulled myself together and started doing
some research of my own. By chance, I came across a report about
a very similar skin condition. A man had contracted it after taking
antibiotics, and I, too, had had to take a course of antibiotics just a
couple of weeks before my first sore appeared. It occurred to me that
although the sores were on my skin, their appearance might be
related to what was going on inside me. Perhaps the course of
antibiotics was key? Had they somehow affected my gut?
From that moment on, I ceased to treat my skin like the skin of a
person with a dermatological problem and began to see it as the skin
of a person with an intestinal condition, though just what that
condition might be, I did not know. I decided to cover all the bases. I
stopped eating dairy products, cut out gluten almost entirely,
swallowed various bacterial cultures, and generally improved my
diet. I also carried out some pretty crazy experiments on myself. If I
had already been studying medicine at that time, I wouldn’t have
dared do half of them. Once, I overdosed on zinc for several weeks,
causing me to have an extremely heightened sense of smell for the
next few months.
With a few tricks, I finally managed to get my condition under
control. This success gave me a lift, and I experienced with my own
body that knowledge is power. That’s when I started studying
medicine.
In my first semester as a student, I was at a party where I ended
up sitting next to a guy who had the smelliest breath I have ever
smelled. It wasn’t a typical bad-breath smell—not the scratchy
hydrogen-breath odors of stressed-out middle-aged gentlemen nor
the sugary, fetid funk from the mouth of an elderly aunt with too
sweet a tooth. After a while, I moved away and sat somewhere else.
The next day, he was dead. He had killed himself. I couldn’t get him
out of my mind. Was there a way his gut might have contributed to
this? Just like my skin condition, which at first appeared unrelated?
Now I had some experience in medical school, I wondered if it could
have been a diseased gut creating that smell, and if so, could a
diseased gut also have affected that man’s psychological state?
A week later, I decided to share my suspicion with a good friend.
And a few months after that, the same friend contracted a bad case
of gastroenteritis, which left her feeling very poorly. The next time we
met, she told me she thought there might be something in my theory,
as her illness had made her feel worse than she ever had felt before,
psychologically as well as physically. Her comments inspired me to
start looking more closely at this subject matter.
Soon, I discovered there was an entire branch of medical
research investigating the links between the gut and the brain. It’s a
rapidly growing field of study. Ten or so years ago, there were hardly
any published studies on the subject; now there are several hundred
academic articles covering the field. The influence of the gut on our
health and well-being is one of the new lines of research in modern
medicine. The renowned American biochemist Rob Knight told the
journal Nature that the field offered at least as much promise as stem
cell research. I had stumbled upon a subject I found more and more
fascinating.
As I continued my medical degree, I got more insight into how my
cesarean birth and lack of breast-feeding might have influenced my
health later in life. I also realized how neglected, even looked down
upon, this area still is in the medical world. This is all the more
surprising when you consider what an extraordinary organ the gut is.
It accounts for two-thirds of our immune system, extracts energy
from sandwiches and vegetarian sausages, and produces more than
twenty unique hormones. Most doctors learn very little about this in
their training. When I visited the Microbiome and Host Health
symposium in Lisbon in May 2013, the number of participants was
modest. About half came from institutions with the financial
wherewithal to allow them to be among the pioneers, including
Harvard, Yale, Oxford, and the European Molecular Biology
Laboratory (EMBL) at Heidelberg University.
I’m sometimes shocked by the way scientists huddle behind
closed doors to discuss their important research results without
informing the public about them at all. Academic caution is often
preferable to premature publication, but fear can also destroy
opportunities. It is now generally accepted in scientific circles that
people with certain digestive problems often suffer from nervous
disorders of the gut. Their gut then sends signals to the part of the
brain that processes negative feelings, although they have done
nothing bad. Such patients feel uneasy but have no idea why. If their
doctors simply treat them as irrational mental cases, it can be
extremely counterproductive! And this is just one example of why
some research results should be published more quickly.
And that is my aim in writing this book. I want to make new
knowledge available to a broad audience and communicate the
information that scientists bury in their academic publications or
discuss behind closed doors at scientific meetings, while many
ordinary people out there are searching for answers. I know there
are many patients suffering from unpleasant conditions who are
frustrated by the medical world. I can’t offer any panaceas, and
keeping your gut healthy is not a miracle cure for everything, but
what I can do is to show, in an entertaining way, why the gut is so
fascinating, what exciting new research is currently underway, and
how we can use this new knowledge to improve our daily lives.
My medical studies and my doctoral research at the Institute for
Medical Microbiology in Frankfurt, Germany, have given me the skills
to sift and sort scientific data. My own personal experience has
helped me develop the ability to communicate this knowledge to
people. My sister has given me the support I needed to keep me on
the right track—listening to me read aloud from my manuscript and
saying, with a charming grin, “I think you better try that bit again.”
( PART ONE)
GUT FEELING
THE WORLD IS a much more interesting place if we look beyond
what is visible to the naked eye. There is so much more to see! If we
start to look more closely, a tree can be more than a spoon-shaped
thing. In a highly simplified way, “spoon” is the general shape we
perceive when we look at a tree: a straight trunk and a round treetop.
Seeing that shape, our eyes tell us “spoon-like thing.” But there are
at least as many roots beneath the ground as there are branches
above it. Our brain should really be telling us something like
“dumbbell,” but it doesn’t. The brain gets most of its input from our
eyes, and that information is very rarely in the form of an illustration
in a book showing trees in their entirety. So, it faithfully construes a
passing forest landscape as “spoon, spoon, spoon, spoon.”
As we “spoon” our way through life like this, we overlook all sorts
of wonderful things. There is a constant buzz of activity beneath our
skin. We are perpetually flowing, pumping, sucking, squeezing,
bursting, repairing, and rebuilding. A whole crew of ingenious organs
works so perfectly and efficiently together that, in an adult human
being, they require no more energy than a 100-watt light bulb. Each
second, our kidneys meticulously filter our blood—much more
efficiently than a coffee filter—and in most cases they carry on doing
so for our entire lives. Our lungs are so cleverly designed that we
use energy only when we breathe in. Breathing out happens without
any expenditure of energy at all. If we were transparent, we would be
able to see the beauty of this mechanism: like a wind-up toy car, only
bigger, softer, and more lung-y. While some of us might be sitting
around thinking “Nobody cares about me!”, our heart is currently
working its seventeen-thousandth twenty-four-hour shift—and would
have every right to feel a little forgotten when its owner thinks such
thoughts.
If we could see more than meets the eye, we could watch as a
clump of cells grows into a human being in a woman’s belly. We
would suddenly see how we develop, roughly speaking, from three
tubes. The first tube runs right the way through us, with a knot in the
middle. This is our cardiovascular system, and the central knot is
what develops into our heart. The second tube develops more or
less parallel to the first along our back. Then it forms a bubble that
migrates to the top end of our body, where it stays put. This tube is
our nervous system, with the spinal cord, including the brain, at the
top and myriad nerves branching out into every part of our body. The
third tube runs through us from end to end. This is our intestinal tube
—the gut.
The intestinal tube provides many of the furnishings of our
interior. It grows buds that bulge out farther and farther to the right
and left. These buds will later develop into our lungs. A little bit lower
down, the intestinal tube bulges again and our liver has begun to
develop. It also forms our gall bladder and pancreas. But, most
importantly, the tube itself begins to grow increasingly clever. It is
involved in the complex construction of our mouth, creates our
esophagus, with its ability to move like a break dancer, and develops
a little stomach pouch so we can store food for a couple of hours.
And, last but not least, the intestinal tube completes its masterpiece
—the eponymous intestine or gut.
The masterpieces of the other two tubes—the heart and the brain
—are generally held in high regard. We see the heart as central to
life since it pumps blood around the body. The brain is admired for its
ability to create a dazzling array of new mental images and concepts
every second. But the gut, in most people’s eyes, is good for little
more than going to the toilet. Apart from that, people think, it just
hangs around inside our bellies, letting off a little “steam” every now
and then. People do not generally credit it with any particular
abilities. It would be fair to say that we underestimate our gut. To put
it more bluntly, we don’t just underestimate it, we are ashamed of it—
more “guilt feeling” than “gut feeling”!
I hope this book will change that by making use of the wonderful
ability that books possess to show us more than the world we see
around us. Trees are not spoons, and the gut is our body’s most
underrated organ. This is its inside story.
How Does Pooping Work? And Why
That’s an Important Question
MY FLATMATE WANDERED into the kitchen one day, saying, “Giulia, you
study medicine—so how does pooping work?” It probably wouldn’t
be a great idea for me to begin my autobiography with that question,
but that little query did literally change my life. I withdrew to my room,
sat on the floor, and was soon poring over three different textbooks.
The answer I eventually discovered left me flabbergasted. This
unspectacular daily necessity turned out to be far more sophisticated
and impressive than I ever would have imagined.
Every time we go to the toilet, it’s a masterly performance—two
nervous systems working tirelessly in tandem to dispose of our
waste as discreetly and hygienically as possible. Very few other
animals do their business in such an admirable and orderly manner.
Our bodies have developed all sorts of mechanisms and techniques
to help us poop properly. The first surprise is the sophistication of our
sphincters. The vast majority of people are familiar only with the
outer sphincter: the muscle we can consciously control, opening and
closing it at will. There is another, very similar muscle close by—but
this is one we can’t control consciously.
Each of the two sphincters looks after the interests of a different
nervous system. The outer muscle is a faithful servant of our
consciousness. When our brain deems it an unsuitable time to go to
the toilet, the external sphincter obeys and stays closed with all its
might. The internal sphincter represents our unconscious inner
world. Whether Great-Aunt Bertha approves of breaking wind or not
is no concern of the sphincter ani internus. It is only interested in
making sure everything is okay inside us. Is the gas pressure rising?
The inner sphincter’s mission is to keep all unpleasantness at bay. If
it had its way, Great-Aunt Bertha would break wind more often. The
main thing for the internal sphincter is to keep everything
comfortable and in its place.
These two sphincter muscles have to work as a team. When
what’s left of our food reaches the internal sphincter, that muscle’s
reflex response is to open. But it does not just open the floodgates
and let everything out, leaving the outer sphincter to deal with the
deluge. First, it allows a small “taster” through. The space between
the internal and external sphincter muscles is home to a large
number of sensor cells. They analyze the product delivered to them,
test it to find out whether it is solid or gaseous, and send the
resulting information up to the brain. This is the moment when the
brain realizes, “It’s time to go to the toilet!” Or maybe, “It’s just a bit of
wind.” It then does what it is so good at with its conscious
awareness: it adapts to the environment we find ourselves in. It
compares the information it receives from our eyes and ears to the
data in its memory bank of past experience. In this way, the brain
takes just a matter of seconds to make an initial assessment of the
situation and send a message back to the sphincter: “I’ve had a look
and we’re at Great-Aunt Bertha’s, in the living room. We might get
away with breaking a little wind if we can squeeze it out silently—
anything more solid might not be such a good idea.”
The external sphincter gets the message and dutifully squeezes
itself closed even more tightly than before. The internal sphincter
receives this signal from its more outgoing partner and respects the
decision—for now. The two muscles work together and maneuver
the taster back into a holding pattern. Of course, it will have to come
out sooner or later, just not here and not now. After a while, the
internal sphincter will simply give it a try with another little taster. If by
then we’re back within our familiar four walls, it’s full steam ahead!
Our internal sphincter is a no-nonsense little guy. His motto is “If
it’s gotta come out, it’s gotta come out!” Not much room for argument
there. The external sphincter, on the other hand, has to deal with the
vagaries of the outside world and its many options. It might,
theoretically, be possible to use this stranger’s toilet, but is that a
good idea? Have my new girlfriend/boyfriend and I been together
long enough for farting in front of each other to be okay—and if so, is
it down to me to break the ice and go first? If I don’t go to the toilet
now, can I wait until this evening or will I get caught short?
The considerations of our sphincter may not sound worthy of a
Nobel Prize, but in fact they are concerned with some of the most
basic questions of human existence: how important to us is our inner
world, and what compromises should we make to get by in the
external world? There are those who clench with all their might to
keep the wind in, come what may, eventually struggling home
wracked with bellyache. Others get Granny to pull on their finger at a
family party, making a funny, if slightly inappropriate, magic show out
of their need to break wind. The best compromise is probably
somewhere in the middle.
If we suppress our need to go the toilet too often or for too long,
our internal sphincter begins to feel browbeaten. In fact, we are able
to reeducate it completely. That means the sphincter and the
surrounding muscles have been disciplined so often by the external
sphincter that they become cowed. If communication between the
two sphincters breaks down completely, constipation can result.
Even without such defecatory discipline, something very similar
can happen to women during labor. Childbirth can cause tearing of
the delicate nerve fibers that allow the two muscles to communicate
with each other. The good news is that those nerves can heal and
reconnect. Irrespective of whether the damage was caused by
childbirth or in some other way, one good treatment option is what
doctors call biofeedback therapy. Biofeedback therapy is offered by
some gastroenterologists or gastroenterology departments. It
teaches the two sphincters to overcome their estrangement and get
to know each other again. A machine is used to measure how
efficiently the internal and external sphincters are working together. If
messages from one to the other get through, the patient is rewarded
with a sound or light signal. It’s like one of those quiz shows on earlyevening television, where the whole set lights up and fanfares blare
when a contestant gets the answer right—only it’s at a medical
practice, not on television, and the “contestant” has a sensor
electrode up his or her butt. That may seem extreme, but it’s worth it.
When the two sphincters are talking properly to each other again,
going to the little girls’ or little boys’ room is an altogether more
pleasant experience.
Sphincters, sensor cells, consciousness, and electrode-up-thebutt quiz shows. My flatmate was probably not expecting all that in
answer to his casual question about pooping, nor did the group of
rather prim female business studies students who had meanwhile
gathered in the kitchen for his birthday party. Still, the evening turned
out to be fun, and it made me realize that a lot of people are actually
interested in the gut. Some interesting new questions were raised at
the birthday party. Is it true that we don’t sit on the toilet properly?
How can we burp more easily? Why can we get energy from steaks,
apples, or fried potatoes, for example, but cars are much more
restricted in their fuel options? Why do we have an appendix? Why
are feces always the same color?
My flatmates have learned to recognize the familiar look on my
face when I rush into the kitchen, bursting to tell them my latest gut
anecdote—like the one about the tiny squat toilets and luminous
poop.
Are You Sitting Properly?
idea to question your own habits from time to time. Are
you really taking the shortest and most interesting route to the bus
stop? Is that comb-over to hide your increasing bald patch elegant
and chic? Or, indeed, are you sitting properly when you go to the
toilet?
There will not always be a clear, unambiguous answer to every
question, but a little experimentation can sometimes open up whole
new vistas. That is probably what was going through the mind of Dov
Sikirov when the Israeli doctor asked twenty-eight test subjects to do
their daily business in three alternative positions: enthroned on a
normal toilet; half-sitting, half-squatting on an unusually low toilet;
and squatting with no seat beneath them at all. He recorded the time
they took in each position and asked the volunteers to assess the
degree of straining their bowel movements had required. The results
were clear. In a squatting position, the subjects took an average of
50 seconds and reported a feeling of full, satisfactory bowel
IT’S A GOOD
emptying. The average time when seated was 130 seconds and the
resulting feeling was deemed to be not quite so satisfactory.
Why the difference? The closure mechanism of our gut is
designed in such a way that it cannot open the hatch completely
when we are seated. There is a muscle that encircles the gut like a
lasso when we are sitting or, indeed, standing, and it pulls the gut in
one direction, creating a kink in the tube. This mechanism is a kind
of extra insurance policy, in addition to our old friends, the
sphincters. Some people will be familiar with this kinky closing
mechanism from their garden hose. You ask your sister to check why
there’s no water coming out of the hose. When she peers down the
end, you quickly unbend the kink, and it’s just a few minutes until
your parents ground you for a week.
But back to our kinky rectal closure mechanism: it means our
feces hit a corner. Just like a car on the highway, turning a corner
means our feces have to put on the brakes. So, when we are sitting
or standing, our sphincters have to expend much less energy
keeping everything in. If the lasso muscle relaxes, the kink
straightens, the road ahead is straight, and the feces are free to step
on the gas.
Squatting has been the natural defecation position for humans
since time immemorial. The modern sitting toilet has existed only
since indoor sanitation became common in the late eighteenth
century. But such “cavemen did it that way” arguments are often met
with disdain by the medical profession. Who says that squatting
helps the muscle relax better and straightens the feces highway?
Japanese researchers fed volunteers luminous substances and Xrayed them while they were doing their business in various positions.
They found out two interesting things. First, squatting does indeed
lead to a nice, straight intestinal tract, allowing for a direct, easy exit.
Second, some people are nice enough to let researchers feed them
luminous substances and X-ray them while they have a bowel
movement, all in the name of science. Both findings are pretty
impressive, I think.
Hemorrhoids, digestive diseases like diverticulitis, and even
constipation are common only in countries where people generally
sit on some kind of chair to pass their stool. This is due not to lack of
tissue strength, especially in young people, but to the fact that there
is too much pressure on the end of the gut. Some people tend to
tense up all their abdominal muscles when they are stressed. Often,
they don’t even realize they are doing it. Hemorrhoids prefer to avoid
internal pressure like that by dangling loosely out of the anus.
Diverticula are small light-bulb-shaped pouches in the bowel wall,
resulting from the tissue in the gut bulging outward under pressure.
Of course, the way we go to the toilet is not the only cause of
hemorrhoids and diverticula; however, it remains a fact that the 1.2
billion people in this world who squat have almost no incidence of
diverticulosis and far fewer problems with hemorrhoids. We in the
West, on the other hand, squeeze our gut tissue until it comes out of
our behinds and we have to have it removed by a doctor. Do we put
ourselves through all that just because sitting on a throne is more
“civilized” than silly squatting? Doctors believe that straining too
much or too often on the toilet can also seriously increase the risk of
varicose veins, a stroke, or defecation syncope—fainting on the
toilet.
A text message I received from a friend who was on holiday in
France read, “The French are crazy! Someone’s stolen the toilets
from the last three service stations we stopped at!” I had to laugh,
first, because I suspected my friend was actually being serious, and
second, because it reminded me of my first experience of French
squat toilets. “Why am I being forced to squat here when you could
just as easily have put in a proper toilet?” I mournfully complained to
myself as I recovered from the shock of the emptiness I saw before
me. Throughout much of Asia, Africa, and southern Europe people
squat briefly over such toilets in a kind of martial arts or downhill
skiing pose to defecate. We, by contrast, take so long, we have to
while away the time until we’ve finished our business with reading
the paper, carefully prefolding pieces of toilet paper for imminent
use, scanning the corners of the bathroom to see if they could do
with a clean, or staring patiently at the opposite wall.
When I read this chapter out to my family in our living room, I
looked up to see disconcerted faces. Are we going to have to
descend from our porcelain thrones and squat precariously over a
hole to poop? Of course not, hemorrhoids or no hemorrhoids! That
said, it might be fun to try climbing up onto the toilet seat to do our
business while squatting there. But there’s no need for that, either. It
is possible to squat while sitting. It’s a particularly good idea when
things don’t come so easily, so to speak. To do it, just incline your
upper body forward slightly and put your feet on a low footrest
placed in front of the toilet, et voilá!—all the angles are correct, and
you can read the paper, prefold your tissue, or stare at the wall with
a clear conscience.
The Gateway to the Gut
YOU MIGHT THINK that the back end of the gut has so many surprises
in store for us because it is something we do not think about very
much. But I don’t think that’s the real reason. The other end of the
gut, the gateway, so to speak, also has no shortage of surprises in
store—even though we are directly confronted with it every morning
when we clean our teeth.
You can seek out these secrets with your tongue. These are four
small points in your mouth. Two of them are located on the inside of
your cheeks, opposite your upper molars, more or less in the middle.
If you explore the area with your tongue, you will feel two tiny bumps.
If they notice them at all, most people assume they must have bitten
themselves in the cheek at some point, but they haven’t. These little
nubs, which doctors call the parotid papillae, are found in the same
position in everybody’s mouth. The other two points are lurking
beneath your tongue, just to the right and left of the lingual frenulum,
the fold of skin connecting your tongue to the floor of your mouth.
These four little nubs supply your mouth with saliva.
The papillae in your cheeks secrete saliva whenever it’s needed
right away—for example, when we eat. The two tiny openings under
the tongue secrete saliva continuously. If you could somehow enter
these channels and swim against the tide of saliva, you would
eventually reach the main salivary glands. They produce the most
saliva—about 11/2 to 2 US pints (0.7 to 1 liter) a day. If you feel
upward from your neck to your cheek, you will notice two soft, round
raised areas. May I introduce you? They are the bosses.
those two constant suppliers of saliva, are
situated right behind our lower front teeth, which are particularly
susceptible to the buildup of tartar. This is because there are
substances in our saliva that contain calcium whose sole function it
is to make our teeth harder. But if a tooth is constantly bombarded
with calcium, it can be a case of too much of a good thing. Tiny
molecules floating innocently by are caught up and “fossilized”
without so much as a by-your-leave. The problem is not the tartar
itself, but the fact that it has such a rough surface, affording a much
better foothold for bacteria that cause tooth decay and gum disease
than smooth, clean tooth enamel.
But what are fossilizing, calcium-containing substances doing in
our saliva? Saliva is basically filtered blood. The salivary glands
sieve the blood, keeping back the red blood cells, which are needed
in our arteries, not in our mouth. But calcium, hormones, and some
products of our immune system enter the saliva from the blood. That
THE SUBLINGUAL PAPILLAE,
explains why each person’s saliva is slightly different. In fact, saliva
analysis can be used to test for diseases of the immune system or
for certain hormones. The salivary glands can also add extra
substances, including those calcium-containing compounds, and
even natural painkillers.
Our saliva contains one painkiller that is stronger than morphine.
It is called opiorphin and was only discovered in 2006. Of course, we
produce only small amounts of this compound, otherwise we would
be spaced out on our own spit all the time! But even a small amount
has a noticeable effect, since our mouth is such a sensitive thing. It
contains more nerve endings than almost anywhere else in the
human body. Even the tiniest strawberry seed can drive us crazy if it
gets stuck somewhere. We feel every grain of sand in a badly
washed salad. A teeny little sore, which we would not even notice if it
were on our elbow, hurts like hell and feels monstrously big in our
mouth—without our salivary painkiller, it would feel even worse!
When we chew, we produce more saliva and with it more of such
analgesic substances, which explains why a sore throat often feels
better after a meal and even minor sores in the oral cavity hurt less.
It doesn’t have to be a meal—even chewing gum provides us with a
dose of our oral anodyne. There are even a handful of new studies
showing that opiorphin has antidepressant properties. Is our spit
partly responsible for the reassuring effects of comfort eating?
Medical research into both pain and depression may deliver the
answers in the next few years.
Saliva protects the oral cavity not only from too much pain, but
also from too many bad bacteria. That’s the job of mucins, for
example. Mucins are proteins that form the main constituent of
mucus. They help provide hours of fascination and fun for young
children who have just found out they can blow bubbles with their
own spit. A more useful function is their ability to envelop our teeth
and gums in a protective mucin net. We shoot them out of our
salivary papillae like Spider-Man shoots webs from his wrists. These
microscopic nets can catch bacteria before they have a chance to
harm us. While the bad bacteria are caught in the net, antibacterial
substances in our saliva can kill them off.
Like the natural painkillers in our saliva, bactericidal substances
are present in our saliva in small concentrations. Our spit is not
supposed to disinfect us completely. In fact, we actually need a core
team of good little creatures in our mouth. Benign bacteria in the
mouth are not totally wiped out by our disinfectant saliva since they
take up space—space that could otherwise be populated by more
dangerous germs.
When we are asleep, we produce very little saliva. That’s good
news for those who tend to drool into their pillow. If they produced
the full daytime quota of 2 to 3 US pints (1 to 1.5 liters) during the
night, too, the results would not be particularly pleasant. The fact that
we produce so little saliva at night explains why many people have
bad breath or a sore throat in the morning. Eight hours of scarce
salivation means one thing for the microbes in our mouth—party
time! Brazen bacteria are no longer kept in check, and the mucus
membranes in our mouth and throat miss their sprinkler system.
That is why brushing your teeth before you go to bed at night and
after you get up in the morning is such a clever idea. Brushing at
bedtime reduces the number of bacteria in your mouth, leaving fewer
partygoers for the all-night bash. Brushing in the morning is like
cleaning up after the party the night before. Luckily, our salivary
glands wake up at the same time we do in the morning and start
production straight away. Munching on our first piece of toast or
performing our morning dental hygiene duties adds extra stimulation
for salivation, and this washes away the nocturnal microbes or
transports them down into our stomach, where our gastric juices
finish them off.
Those who suffer from bad breath during the day may have not
managed to remove enough musty-smelling bacteria. Those cunning
little critters love to hide out under the newly formed mucin net,
where the antibacterial substances in our saliva cannot get to them.
A tongue scraper can help here, but so can chewing gum, which
helps stimulate saliva production to swill out those mucin hideouts. If
none of this helps, there is another place where the causes of bad
breath can lurk—but more of that later, after we have found out
about the second secret place in our mouth.
This place is one of those typical surprises—like when you think
you know someone, only to find out they have an unexpected crazy
side to them. The well-coiffed secretary from Chicago who turns up
on the Internet as a fanatical ferret breeder. The heavy-metal
guitarist seen buying skeins of yarn because he finds knitting so
relaxing and it’s such a good workout for the fingers. The best
surprises come after first impressions have been made, and the
same is true of your own tongue. When you look in the mirror and
stick out your tongue, you are not seeing it in all its glory. You might
well ask how it looks farther down, as you can clearly see that it does
not just end at the back of your mouth. In fact, the root of the tongue
is where things start to get really interesting.
The root of the tongue is home to an alien landscape of pink
domes. Those whose gag reflex is not too pronounced can carefully
feel the root of their tongue with a finger. When you reach the root,
you will notice it gets pretty bumpy back there. The job of these
nodules—doctors call them your lingual tonsils—is to investigate
everything we swallow. To do this, they pick up tiny particles of
anything we eat, drink, or inhale and draw them into the nodule.
Inside, an army of immune cells waits to receive training in how to
deal with foreign substances invading from the outside world. They
need to learn to leave bits of apple in peace, while attacking anything
that might give us a sore throat. So, if you do explore the root of your
tongue with your finger, it is not clear who is explorer and who the
explored. After all, this area includes some of the most inquisitive
tissue in our body—immune tissue.
The immune tissue at the base of the tongue, also called the lingual tonsils.
The immune tissue has a number of such inquisitive hotspots.
Strictly speaking, a ring of immune tissue encircles our entire throat.
Known to scientists as Waldeyer’s tonsillar ring, it includes those
lingual tonsils at the bottom of the circle; the palatine tonsils—these
are the ones we generally think of as our tonsils—at either side; and
at the top of the ring, where the ear, nose, and throat areas meet,
there is more such tissue. (When swollen and infected, especially in
children, this is what we know as adenoids.) Those who believe they
have no tonsils left are not quite correct. The entire collection of
tissue in Waldeyer’s ring makes up our tonsils. Whether they are
located at the root of the tongue, at the back of the mouth, or at the
side of our throat, all these areas of tonsillar tissue do the same job:
they inquisitively investigate any foreign substance they encounter
and use the information to train the immune system to defend us.
The tonsils—the ones we often have removed—are just not as
clever in the way they go about this task. Rather than forming
bumps, they tend to form deep grooves (to increase surface area)
known rather spookily as “crypts.” Sometimes, too much foreign
material can get caught in the crypts, leading to frequent infections.
This is a side effect, so to speak, of having overinquisitive tonsils.
So, if the tongue and teeth have been excluded as a cause of a
patient’s bad breath, the next place to check is the tonsils—if they
are still there.
Sometimes, little white stones can be found hiding in the crypts,
and these stones smell terrible! Often, people have no idea they are
there, and they spend weeks trying unsuccessfully to get rid of bad
breath or a strange taste in their mouth. No amount of tooth
brushing, tongue scraping, or gargling helps. The little stones will
eventually work their way out of their hiding places, with no
permanent harm done. But you can also take fate into your own
hands and, with a little practice, squeeze them out. That done, bad
breath problems disappear instantaneously.
The best test to find out whether smelly breath is caused by
these little deposits is simply to run a finger or a cotton bud over the
tonsils and then sniff it. If it smells unpleasant, it is time to go hunting
for tonsil stones. Ear, nose, and throat doctors can also remove
them, which is the safer and more convenient option. Those with a
strong stomach and a love of barely watchable videos can visit
YouTube to see various techniques for squeezing tonsil stones out
and view some extreme examples. But be warned! These videos are
not for the fainthearted.
There are also other household remedies for tonsil stones. Some
people gargle with salt water several times a day; others swear by
fresh, raw sauerkraut from the health-food store; and yet others
claim cutting out dairy products will prevent them from forming.
There is no scientific basis for any of these remedies. A more
thoroughly researched medical question is that of when a
tonsillectomy can or should be carried out. The answer turns out to
be—not before the age of seven.
Seven is the age by which we have probably seen it all, or all that
is important for our immune cells: being born into a completely
unfamiliar world; being kissed and cuddled by Mom; playing in the
garden or the woods; touching animals; having many colds in quick
succession; meeting a load of new people at school. And that’s
about it. By this time, our immune system has finished its schooling,
so to speak, and can go to work for us for the rest of our life.
Before we reach the age of seven, our tonsils are still an
important training camp for our immune cells. Building a healthy
immune system is not only important for warding off colds, it also has
an important part to play in keeping our heart healthy and in
controlling our body weight. For example, removing the tonsils of a
child younger than seven can lead to an increased risk of obesity.
Why this should be the case is something doctors have not yet
discovered. However, more and more researchers are now
becoming interested in the link between the immune system and
body weight. This tonsil-tubbiness effect can be a boon for
underweight children because the associated weight gain can propel
them into the normal weight range, but for all other children, parents
are best advised to make sure their child eats a healthy, balanced
diet after a tonsillectomy.
So the tonsils of children below the age of seven should stay in,
unless there is a very good reason for taking them out. If the tonsils
are so large that they impede normal breathing or sleeping, for
example, the tonsil-tubbiness effect is secondary. It may seem sweet
of our immune tissue to want to defend us so loyally, but in such
cases, it does more harm than good. Often, doctors can use lasers
to remove only that part of the tonsils that is causing the trouble.
They no longer have to leave patients completely tonsil-less. Chronic
or repeated infections are a different story altogether. In such cases,
our immune cells are kept constantly busy, with no time for a bit of
R&R, and that is not good for them if it continues for too long.
Whether we are four, seven, or fifty years old, an oversensitive
immune system can benefit from saying goodbye to those tonsils.
One example of those who benefit from having their tonsils
removed is psoriasis sufferers. In psoriasis, an overreaction of the
immune system causes itchy skin lesions—often starting at the head
—and painful inflammation of the joints. Psoriasis patients also have
an above-average vulnerability to sore throats. One possible factor in
this is bacteria, which can hide in the tonsils for long periods of time
and needle the immune system from there. For more than thirty
years, doctors have described cases of psoriasis patients whose
skin condition improved or cleared up entirely following a
tonsillectomy. In 2012, this prompted researchers from Iceland and
the United States to investigate the phenomenon more closely. They
split twenty-nine psoriasis patients who also suffered frequent sore
throats into two groups. One group had their tonsils surgically
removed, the other didn’t. Thirteen of the fifteen “detonsilized”
patients reported a significant long-term improvement in their skin.
Those still in possession of their tonsils reported little or no change.
Some sufferers of rheumatic diseases are also now advised to have
their tonsils removed if they are suspected of being part of the cause
of the condition.
Tonsils in or tonsils out? There are good arguments for both.
Those forced to bid farewell to their tonsils at an early age need not
worry that their immune system has missed an important lesson from
the oral cavity. Luckily, there is still all the rest of the tissue at the
base of the tongue and back of the throat. And those whose tonsils
are still in place need not worry that they have been left with nothing
but a trap for bacteria. Many people’s tonsillar crypts are quite
shallow and so are less likely to cause problems for their owners.
The other parts of Waldeyer’s ring are actually very bad at providing
a refuge for bacteria: they are constructed differently and have
glands to help them clean themselves regularly.
There is something happening every second in our mouth:
salivary papillae shoot out nets of mucin, take care of our teeth, and
protect us from the effects of oversensitivity. Our tonsillar ring keeps
watch for foreign particles and uses them to train its immune army.
But we would need none of this if the story didn’t continue beyond
our mouth. The mouth is simply the gateway to a world where the
external becomes internalized.
The Structure of the Gut
SOME THINGS TURN out to be a disappointment once you get to know
them better. Those chocolate wafers from the television commercial
are not lovingly hand-baked by housewives in country dresses—they
come from a factory with neon strip lighting and workers at
production lines. School turns out to be much less fun than you
thought it would be on the first day. It’s warts and all in the backstage
area of life, where there is a lot that looks much better from a
distance than up close.
That is not the case for the gut, however. Our intestinal tube
looks rather odd from a distance. Beyond the mouth, a 1-inch- (2centimeter-) wide esophagus, or gullet, leads down from the throat,
misses the top of the stomach, and passes into it somewhere at the
side. The right-hand side of the stomach is much shorter than the
left, which is why it curls up into a crescent-shaped, lopsided pouch.
The small intestine meanders with no particular sense of direction,
sometimes to the right, sometimes to the left, for all its length (about
20 feet, or 6 meters) until it eventually passes into the large intestine.
That’s where we find the apparently useless appendix, which seems
to be incapable of doing anything except getting infected. The large
intestine is also full of bulges. In fact, it looks a little like a sorry
attempt to replicate a string of beads. Seen from a distance, the gut
is an unsightly, charmless, asymmetrical tube.
So, let’s forget the view from a distance and zoom in for a closer
look. There is scarcely another organ in our body that becomes
increasingly fascinating the closer you get. And, the more you know
about the gut, the more beautiful it appears. So, let’s look at some of
those strange structures a little more closely.
The Lanky Esophagus
we notice about this long, slender organ is that it can’t
aim properly. Rather than taking the shortest route and aiming for the
middle of the stomach, it enters the organ on the right-hand side.
This is a smart move. Surgeons would call such a connection
terminolateral. It may mean taking a little detour, but it’s well worth it.
When simply walking normally, we tense our abdominal muscles,
doubling the pressure in our abdomen with every step we take.
When we laugh or cough, for example, that pressure increases by
several times. Since the abdomen presses against the stomach from
below, it would be a bad idea for the esophagus to dock directly onto
the top end of the stomach. Connected as it is at the side, it has to
deal with only a fraction of the pressure. It is thanks to this
arrangement that we can take a walk after a heavy meal without
having to burp with every step. This clever angle and its closing
mechanism are also to thank for the fact that, although a fit of
laughter might result in us losing a little control over our outer
sphincter and inadvertently letting out a little “laughing gas,” few
people have been known to vomit from laughing.
A side effect of this lateral connection is the so-called gastric
bubble. This small bubble of air at the top of the stomach can be
seen clearly on X-rays. Air rises vertically, after all, and does not
search out a side exit. This bubble is the reason many people find
they have to swallow a little air in order to burp. This swallowing
motion moves the opening of the esophagus a little closer to the
bubble, and—hey presto!—the burp can make its upward journey to
THE FIRST THING
freedom. Those who need to burp while lying down can make the
process easier by lying on their left side. So, if you’re kept awake at
night by a bloated stomach and you are lying on your right side, the
best thing to do is simply to turn over.
In order better to illustrate the stomach bubble, this illustration does not show the correct
distribution of black and white in a normal X-ray image. Normally, denser materials, such as
teeth or bone, show up white, while less dense materials, such as the stomach bubble or
the air in the lungs, show up as dark areas.
The lanky appearance of the esophagus is also more beautiful
than it seems at first glance. Looking very closely, it can be seen that
some muscle fibers run around the esophagus in a spiral pattern.
They are the reason for its elasticity. If you extend these fibers
lengthways, they constrict spirally, like a telephone receiver cable.
Bundles of fibers connect the esophagus to the spinal column.
Sitting up straight and looking upwards stretches the esophagus
along its length. This causes it to narrow, in turn allowing it to close
more efficiently at each end. That is why sitting or standing up
straight can help prevent heartburn after a large meal.
The Lopsided Stomach Pouch
much higher in our abdomen than we think. It
begins just below the left nipple and ends below the bottom of the
ribcage on the right. Any pain felt farther down than this lopsided
little pouch cannot be stomachache. Often, when people say they
have stomach problems, the trouble is actually in the gut. The heart
and the lungs sit on top of the stomach. This explains why we find it
more difficult to breathe deeply after eating a lot.
One condition often overlooked by general practitioners and
family doctors is Roemheld syndrome, when so much gas collects in
the stomach that it presses up against the heart and the nerves in
the gut. Sufferers can display a range of different symptoms,
including dizziness and discomfort. In more severe cases, Roemheld
syndrome can cause anxiety or difficulty in breathing, and may also
OUR STOMACH SITS
lead to severe chest pain that feels like a heart attack. Doctors often
write off undiagnosed Roemheld sufferers as overanxious
malingerers whose symptoms are all in their mind. A more useful
approach would be to ask patients if they have tried burping or
passing wind. In the long term, it may be better for such patients to
avoid any food that leaves them bloated or flatulent, take measures
to restore the balance of the stomach or gut flora, and avoid drinking
alcohol to excess. Alcohol can multiply the number of gas-producing
bacteria by a factor of up to a thousand. In fact, some bacteria feed
on alcohol (which is why rotten fruit tastes alcoholic). With a gut full
of busy gas producers, a night on the town can lead to a morning
chorus of the pungent kind. So much for the “alcohol is a
disinfectant” argument!
Now let us turn to the stomach’s strange shape. One side is
much longer than the other and so the entire organ has to bend
double. That creates large folds inside it. The stomach could be
called the Quasimodo of the digestive organs. But its misshapen
appearance has a deeper meaning. When we take a drink of water,
the liquid can flow straight down the shorter, right-hand side of the
stomach to end up at the entrance to the small intestine. Food, on
the other hand, plops against the larger side of the stomach. Our
digestive pouch cunningly separates the substances it still needs to
work on to break them down, from the fluids that it can wave straight
on through to the next digestive station. So our stomach is not simply
lopsided; rather, it has two sides with different specializations. One
side copes better with fluids, the other with solids. Two stomachs for
the price of one, so to speak.
The Meandering Small Intestine
meanders about in our abdominal cavity, twisting
and turning for a distance of between 10 and 20 feet (3 and 6
meters). If we bounce on a trampoline, it bounces along with us.
When the plane we’re sitting on takes off, it is pressed into the back
of the seat like the rest of us. When we dance, it merrily wobbles
along to the music, and when abdominal pain makes us wince, its
muscles wince in a similar way.
There are few people in the world who have seen their own small
intestine. Even doctors usually examine only the large intestine when
they perform a colonoscopy. But those who do get the rare
opportunity of seeing their small intestine by swallowing a pill-sized
camera are likely to be surprised. Most expect to encounter a
gloomy tunnel, but what they see is a very different creature: moist,
pink, with a velvety sheen and somehow delicate looking. Most
people do not realize that only the final three feet or so (about the
last meter) of our large intestine has anything to do with feces—the
preceding sections of our intestinal tract are surprisingly clean (and
largely smell-free, incidentally). Our gut faithfully and tastefully takes
on everything we swallow down to it.
At first sight, the small intestine seems rather more haphazard in
its design than our other organs. The heart has its four chambers,
the liver has its lobes, veins have valves, and the brain has
specialized areas—but the small intestine just wanders aimlessly
about in our abdomen. Its true design becomes clear at the
microscopic level. We have here a creature that epitomizes the
phrase “love of detail.”
THE SMALL INTESTINE
Intestinal villi, microvilli, and glycocalyxes. One millimeter (mm) is slightly less than â…Ÿ16 of
an inch.
Our gut wants to offer us as much surface area as possible. That
is why it loves folds—including the folds we can see with the naked
eye. Without folds, our small intestine would need to be up to 60 feet
(18 meters) long to provide us with enough surface area for our
digestion. So, here’s to folds! But a perfectionist like the small
intestine doesn’t stop there. Each square inch of its surface contains
about 20,000 tiny fingerlike projections (or about 30 projections per
square millimeter). These projections, called villi by scientists,
protrude out into the mush of partly digested food, the medical word
for which is “chyme.” The villi’s size means they appear as a velvety
structure to the unaided human eye. Under the microscope, the little
villi look like large waves made out of cells. (Velvet looks very similar
under a microscope.) Even greater magnification reveals that each
and every one of those cells is itself covered with little protrusions—
the microvilli: villi on villi, if you like. The microvilli are, in turn,
covered with a velvety meshwork made of countless sugar-based
structures that look a little bit like antlers. These are called the
glycocalyxes. If all this—the folds, the villi, and the microvilli—were
ironed out to a smooth surface, our small intestine would have to be
some 4½ miles (7 kilometers) long.
Why does the small intestine have to be so huge, anyway? In
total, the surface area of our digestive system is about one hundred
times greater than the area of our skin. That seems a little excessive
just to deal with a small portion of fries or a single apple. But this is
what it’s all about inside our belly: we enlarge ourselves as much as
possible in order to reduce anything from outside to the smallest size
we can, until it is so tiny that our body can absorb it and it eventually
becomes a part of us.
We begin that process in the mouth. A bite of an apple sounds
like such a juicy idea because, when we take that bite, our teeth
burst millions of apple cells like tiny balloons. The fresher the apple
is, the more of its cells remain intact—which is why we can tell how
fresh the fruit is by its crispness as we bite into it.
Just as we prefer crisp, fresh fruit, we also love hot, protein-rich
food. We find steak, scrambled eggs, or fried tofu more appetizing
than raw meat, slimy eggs, or cold bean curd. That’s because we
have an intuitive understanding of how digestion works. If we
swallow a raw egg, it will undergo the same processes in our
stomach as it would in the frying pan. The white of the egg turns
opaque, the yolk takes on a pastel color, and both set and become
solid. If we were to vomit the raw egg back up after the right amount
of time, the results would look like almost perfect scrambled eggs—
without any cooking! Proteins react to the heat in the hot pan and the
acid in our stomach in the same way—they unfold. That means they
no longer possess the clever design features that make them soluble
in the liquid of the egg white, so they form solid white lumps. In this
state, they can be digested far more easily in the stomach and the
small intestine. Cooking food saves us the whole first burst of energy
required to unfold those proteins, which would otherwise have to be
expended by the stomach. By preferring cooked food, the body
outsources the first part of the digestive process.
The final breakdown of the food we eat takes place in the small
intestine. Right at the start of this part of the gut there is a small
opening in its wall. This is the duodenal papilla—similar to the
salivary papillae in our mouth, but bigger. It is through this little hole
that digestive juices are squirted onto the chyme. As soon as we eat
something, the liver and pancreas begin to produce these juices and
deliver them to the papilla. These juices contain the same agents as
the laundry detergent and dish soap you can buy from any
supermarket: digestive enzymes and fat solvents. Laundry detergent
is effective in removing stains because it “digests out” any fatty,
protein-rich, or sugary substances from your laundry, with a little help
from the movement of the washing-machine drum, leaving these
substances free to be rinsed down the drain with the dirty water. That
is more or less the same as what happens in our small intestine. The
main difference is that the pieces of protein, fat, or carbohydrates
that are broken down in the intestine ready to be transported to the
bloodstream through the gut wall are huge by comparison. A bite of
an apple is then no longer a bite of apple, but a nutritious pulp made
up of billions and billions of energy-rich molecules. Absorbing them
all requires a huge surface area—a length of 4½ miles (7 kilometers)
is just about enough. That also leaves some space as a safety
buffer, in case parts of the gut are temporarily put out of action by
infection or gastric flu.
Each individual villus contains a tiny blood vessel—a capillary—
that is fed with the absorbed molecules. All the small intestine’s
blood vessels eventually come together and carry the blood to the
liver, where the nutrients are screened for harmful substances and
toxins. Any dangerous substances can be destroyed here before the
blood passes into the main circulatory system. If we eat too much,
this is where the first energy stores are created. The nutrient-rich
blood then flows from the liver directly to the heart. There, it receives
a powerful push and is pumped to the countless cells of our body. In
this way, a sugar molecule can end up in a skin cell in your right
nipple, for example, where it is absorbed and then “burned” along
with oxygen. That releases energy, which the cell uses to stay alive,
with heat and tiny amounts of water created as byproducts. This
happens inside so many cells at the same time that the heat
produced keeps our body at a constant temperature of 97 to 99
degrees Fahrenheit (36 to 37 degrees Celsius).
The basic principle underlying our energy metabolism is simple.
Nature requires energy to ripen an apple on the tree. We humans
come along and break the apple down into its constituent molecules
and metabolize them for energy. We then use the energy released to
keep us alive. All the organs that develop out of that embryonic gut
tube are able to provide fuel for our cells. Our lungs, for example, do
nothing other than absorb molecules with every breath we take.
Thus, “breathing in” really means “taking in nourishment in gaseous
form.” A good proportion of our body weight is made from such
inhaled atoms and not from cheeseburgers. Indeed, plants draw the
majority of their weight from the air and not from the soil they grow in
. . . I hope I haven’t just inadvertently provided the next dubious diet
idea to appear in women’s magazines!
So, all our body’s organs use up energy, but it is from the small
intestine that we start to get some energy back. That explains why
eating is such a pleasant pastime. However, we can’t expect to feel a
burst of energy as soon as we have swallowed the last mouthful of a
meal. In fact, many people find they feel tired and sluggish after
eating. The food has not yet reached the small intestine—it is still in
the preparatory stages of digestion. We no longer feel hungry
because our stomach has been expanded by the food we’ve eaten.
But we feel just as sluggish as we did before the meal, and now we
have to come up with the extra energy for all that mixing and
breaking down. To achieve this, a large amount of blood is delivered
to our digestive organs, and many researchers also believe that
postprandial tiredness may be due to the resulting reduced blood
supply to the brain.
One of my professors always dismissed that idea, arguing that if
all the blood in our head were diverted to our stomach we would be
dead, or at least unconscious. Indeed, there are other possible
causes of the fatigue that follows eating. Certain messenger
chemicals released by the body when we are full can also stimulate
the areas of the brain responsible for tiredness. This tiredness is
perhaps inconvenient for our brain when we are at work, but the
small intestine welcomes it. It works most effectively when we are
pleasantly relaxed. It means the optimum amount of energy is
available for digestion and our blood is not full of stress hormones.
The phlegmatic after-lunch reader is a more efficient digester than
the stressed-out office executive.
The Unnecessary
Appendix
and the Bulgy Large
Intestine
things in life than lying on an examining table at the
doctor’s with one thermometer in your mouth and another in your
behind. But that used to be the standard examination in cases of
suspected appendicitis. A significantly higher temperature down
below than in the mouth was a major indication. Modern doctors no
longer need to rely on temperature differences to diagnose
appendicitis. Important symptoms are fever in combination with pain
below and to the right of the belly button (the position of the
appendix in most people).
Often, pressing that side of the lower abdomen will cause pain,
while, curiously, pressing the other side will relieve it. As soon as
pressure on the left-hand side is released—ouch! This is because
our abdominal organs are surrounded by a supporting fluid. When
pressure is applied to the left-hand side, extra support fluid is pushed
over to the right, where it provides additional cushioning for the
inflamed gut, which relieves pain. Other signs of appendicitis are
pain when raising the right leg against a resistant pressure (get
someone to push against it), lack of appetite, and nausea.
THERE ARE NICER
Our appendix, officially known as the vermiform, or worm-shaped,
appendix, has a reputation for being useless. Looking like a deflated
balloon of the kind children’s party entertainers twist into animal
shapes, the appendix is not only too small to deal with chyme, it is
also positioned in a location that partly digested food hardly ever
reaches. It is just below the junction between the small and large
intestines, and is completely bypassed. This is a creature that can
only look on from below as the world continues on its way above.
Those of you who remember the bumpy landscape in your mouth
might have an idea what its true function could be. Although far
removed from the rest of its kind, the appendix is part of the tonsillar
immune tissue.
Our large intestine takes care of things that cannot be absorbed
in the small intestine. For that reason, it does not have the same
velvety texture. It would simply be a waste of energy and resources
to fill this part of the gut with absorbent villi. Instead, the large
intestine is the home of most of our gut bacteria, which can break
down the last nutritious substances for us. And our immune system
is very interested in these bacteria.
So, the vermiform appendix couldn’t be better placed. It is far
enough away so as not to be bothered by all the digestive business
going on above it, but close enough to monitor all foreign microbes.
Although the walls of the large intestine include large deposits of
immune cells, the appendix is made almost entirely of immune
tissue. So, if a bad germ comes by, it is surrounded. However, that
also means that everything around it can become infected—360degree, panoramic inflammation, so to speak. If this inflammation
causes the appendix to swell, the little tube has problems sweeping
itself clean of those bad germs—leading to one of the more than
270,000 appendectomies carried out every year in the United States
alone.
However, that is not the only function of the appendix. It leaves
only good germs alive and attacks anything it sees as dangerous,
and this also means a healthy appendix acts as a storehouse of all
the best, most helpful bacteria. This was discovered by American
researchers Randal Bollinger and William Parker in 2007. Its
practicality comes into play after a heavy bout of diarrhea. That will
often flush away many of the typical gut microbes, leaving the terrain
free for other bacteria to settle. This should not be left to chance.
And this is when, according to Bollinger and Parker, the appendix
team steps in and spreads out protectively throughout the entire
large intestine.
In most parts of North America and northern Europe, we do not
have many pathogens that cause diarrhea. We may pick up a
gastrointestinal flu bug every now and then, but our environment
teems with much less dangerous microbes than in India or Spain, for
example. So you could say that we do not need our appendix as
urgently as the people in those regions. That means no one in areas
with few diarrhea-inducing pathogens who has undergone an
appendectomy, or is about to face one, should be too worried. The
immune cells in the rest of the large intestine may not be quite so
closely packed, but in total, they are many times more numerous
than those in the appendix, and they are competent enough to take
on the job. Anyone who wants to take no chances after a bout of
diarrhea can buy good bacteria at the pharmacy to repopulate their
gut.
So now, I hope, it is clear why we have an appendix. But what’s
the purpose of the large intestine that it is appended to? Nutrients
have already been absorbed, there are no villi here, and what does
our gut flora want with indigestible leftovers anyway? Our large
intestine does not wind about like its smaller counterpart. It
surrounds our small intestine on the outside, like a plump picture
frame. And it would not take exception to being called plump—it
simply needs more room to do its job.
“Waste not, want not” may sound hackneyed today, but for past
generations it was a way to survive lean times. And it is also the
motto of our large intestine. It takes its time with all the leftovers and
digests them thoroughly. The small intestine can get on with
processing the next meal, or even the next two, in the meantime,
without affecting the large intestine’s work. It doggedly processes
leftovers for sixteen hours or so. In doing so, it makes available
substances that would have been lost if the gut were more hurried.
They include important minerals like calcium, which can only be
absorbed properly here. The careful cooperation of the large
intestine and its flora also provides us with an extra helping of
energy-rich fatty acids, vitamin K, vitamin B12, thiamine (vitamin B1),
and riboflavin (vitamin B2). Those substances are useful for many
things—for example, to help our blood clot properly, to strengthen
our nerves, or to prevent migraines. In the final three feet or so
(about the last meter) of the large intestine, our water and salt levels
are finely tuned. Not that I’m recommending a taste test, but the
saltiness of our feces always remains the same. This fine-balancing
act saves the body an entire quart (or liter) of fluids, which we would
have to make up by drinking that much more per day.
As with the small intestine, all the treasures absorbed by the
large intestine are transported first to the liver for checking, before
entering the main blood system. The final few inches (or
centimeters) of the large intestine, however, do not send their blood
to the detoxifying liver; blood from their vessels goes straight into the
main circulatory system. This is because, generally, nothing more is
absorbed in this section, simply because everything useful has
already been removed. But there is one important exception: any
substances contained in a medical suppository. Suppositories can
contain much less medication than pills and still take effect more
quickly. Tablets and fluid medications often have to contain large
doses of the active agent because much of it is removed by the liver
before it even reaches the area of the body it is meant to act on.
That is, of course, less than ideal, since the substances recognized
by the liver as toxins are the reason we take the medicine in the first
place. So, if you want to do your liver a favor and still need to take
fever-reducing or other medication, make use of the shortcut via the
rectum and use a suppository. This is an especially good idea for
very young or very old patients.
What We Really Eat
THE MOST IMPORTANT phase of our digestion takes place in the small
intestine, where the maximum surface area meets the maximum
reduction of our food down to the tiniest pieces. This is where the
decisions are made. Can we tolerate lactose? Is this food good for
our health? Which food causes allergic reactions? Here, in this final
stage of breakdown, our digestive enzymes work like tiny pairs of
scissors. They snip away at our food until it shares a lowest common
denominator with our cells. Canny as ever, Mother Nature here
makes use of the fact that all living things are made out of the same
basic ingredients: sugar molecules, amino acids, and fats.
Everything we eat comes from living things—at this biological level,
there is no difference between an apple, a tree, and a cow.
Sugar molecules can be linked to form complex chains. When
that happens, they no longer taste sweet, and we know them as the
carbohydrates we find in bread, pasta, or rice. After that piece of
toast you ate for breakfast has undergone the snipping of the
enzyme scissors, the final product is the same number of sugar
molecules as a couple of spoonfuls of refined household sugar. The
only difference is that household sugar does not require so much
work from our enzymes as it is already broken down into such small
pieces when it arrives in the small intestine that it can be absorbed
directly into the bloodstream. Eating too much pure sugar at once
really does make our blood sweeter for a while.
The sugar contained in white toast is digested relatively quickly
by our enzymes. With wholegrain bread, everything moves at a
much more leisurely pace. Such bread contains particularly complex
sugar chains, which have to be broken down bit by bit. So,
wholegrain bread is not a sugar explosion, but a beneficial sugar
store. Incidentally, our body has to work much harder to restore a
healthy balance if a sugar onrush comes suddenly. It pumps out
large amounts of various hormones, most importantly insulin. The
result is that we rapidly feel tired again once this special operation is
over. If it doesn’t enter the system too quickly, sugar is an important
raw material for our body. It is used as fuel for our cells—like heatgiving firewood—or to build sugar structures for use in our body,
such as the antler-like glycocalyxes attached to our gut cells.
Despite the problems, our body loves sugary sweet treats
because they save the body work, since sugar can be taken up more
quickly. The same is true of warm proteins. In addition, sugar can be
turned into energy extremely quickly, and our brain rewards us for a
rush of rapid energy by making us feel good. However, there is one
problem: never before, in the history of humankind, have we been
faced with such a huge abundance of readily available sugar. Some
80 percent of the processed foods found on the shelves of modernday American supermarkets contain added sugar. On an
evolutionary scale, then, we could say our species has just
discovered the secret stash of candies at the back of the cupboard,
and it keeps returning to binge on the booty before collapsing on the
couch with a stomachache and sugar shock.
Even though we know intellectually that too much snacking is bad
for us, we can’t really blame our instincts for encouraging us to grab
every opportunity for a treat. When we eat too much sugar, our body
simply stores it away for leaner times. Quite practical, really. One
way the body does this is by relinking the molecules to form long,
complex chains of a substance called glycogen, which is then stored
in the liver. Another strategy is to convert the excess sugar into fat
and store it in fatty tissue. Sugar is the only substance our body can
turn into fat with little effort.
Glycogen reserves are soon used up—just about the time during
your run when you notice the exercise is suddenly much harder
work. That is why nutritional physiologists say we should do at least
an hour’s exercise if we want to burn fat. It is not until we pass
through that first energy dip that we start to tap into those fine
reserves. We might find it annoying that our paunch isn’t the first
thing to go, but our body is deaf to such complaints. The simple
reason for this is that human cells adore fat.
Fat is the most valuable and efficient of all food particles. The
atoms are so cleverly combined that they can concentrate twice as
much energy per ounce as carbohydrates or protein. We use fat to
coat our nerves—just like the plastic on an electric cable. It is this
coating that makes us such fast thinkers. Some of the most
important hormones in our body are made out of fat, and every
single one of our cells is wrapped in a membrane made largely of fat.
Such a special substance must be protected and not squandered at
the first sign of physical exertion. When the next period of famine
comes—and there have been many over the eons—every ounce of
fat in that paunch is a life insurance policy.
Our small intestine also knows the special value of fat. Unlike
other nutrients, it cannot be absorbed straight into the blood from the
gut. Fat is not soluble in water—it would immediately clog the tiny
blood capillaries in the villi of the gut and float on top of the blood in
larger vessels, like the oil on spaghetti water. So fat must be
absorbed via a different route: the lymphatic system. Lymphatic
vessels are to blood vessels as Robin is to Batman. Every blood
vessel inside the body is accompanied by a lymphatic vessel, even
each tiny capillary in the small intestine. While our blood vessels are
thick and red and heroically pump nutrients to our tissues, the
lymphatic vessels are thin and filmy white in color. They drain away
fluid that is pumped out of our tissue and transport the immune cells,
whose job it is to ensure that everything is as it should be throughout
the body.
Lymphatic vessels are so slight because they do not have
muscular walls like our blood vessels. Often, they work just by using
gravity. That explains why we sometimes wake up in the morning
with swollen eyes. Gravity is not very much help when you are lying
down. The tiny lymphatic vessels in our face are nicely open, but it is
only when we get up and gravity kicks in that the fluid transported
there during the night by our blood vessels can flow back down. (The
reason our lower legs do not fill up with fluid after a long day on our
feet is that our leg muscles squeeze the lymphatic vessels every
time we take a step and that squeezes the fluid—known as lymph in
medical circles—upwards.) The lymphatic system is seen as an
underappreciated weakling everywhere in the body except in the
small intestine. This is its time to shine! All the body’s lymph vessels
converge in an impressively thick duct, where all the digested fat can
gather without the risk of clogging.
It’s well known that doctors like to show off their Latin skills, and
they give this vessel the mighty sounding name ductus thoracicus. It
sounds almost as if it means to say, “Hail, Ductus! Teach us why
noble fat is so important and evil fat so bad!” Shortly after we eat a
fatty meal, there are so many tiny fat droplets in our ductus or
thoracic duct that the lymph fluid is no longer transparent but milky
white. When the fat has gathered, the thoracic duct skirts the belly,
passes through the diaphragm, and heads straight for the heart. (All
the fluid drained from our legs, eyelids, and gut ends up here.) So,
whether it’s extra virgin olive oil or cheap fat from french fries, it all
goes straight into the heart—there is no detoxing detour via the liver
as there is for everything else we digest.
A = Blood vessels pass through the liver and then go on to the heart. B = Lymphatic vessels
go straight to the heart.
Detoxification of dangerous, bad fat takes place only after the
heart has given the fat-laden fluid a powerful push to pump it through
the system and the droplets of fat happen to end up in one of the
blood vessels of the liver. The liver contains quite a large amount of
blood, and so the probability is high that such a meeting will take
place sooner rather than later, but before that happens, our heart
and our blood vessels are at the mercy of everything that
McDonald’s and similar fast-food outlets were able to get hold of at
the lowest purchase price.
Just as bad fat can have a negative effect, good fat can work
wonders. Those who are prepared to spend that little bit extra on
cold-pressed (extra virgin) olive oil will be dunking their baguette in a
soothing balm for their heart and blood vessels. Many studies have
been carried out into the effects of olive oil, and results show that it
can protect against arteriosclerosis, cellular stress, Alzheimer’s, and
eye diseases such as macular degeneration. It also appears to have
beneficial effects on inflammatory diseases such as rheumatoid
arthritis and help in protecting against certain kinds of cancer. Of
particular interest to those fighting fat is that olive oil also has the
potential to help get rid of that spare tire. It blocks an enzyme in fatty
tissue—known as fatty acid synthase—that likes to create fat out of
spare carbohydrates. And we are not the only ones who
benefit from the properties of olive oil—the good bacteria in our gut also appreciate a little
pampering.
Good-quality olive oil costs a little bit more. However, it tastes
neither greasy nor rancid, but rather green and fruity, and it
sometimes leaves a peppery feeling in your throat after you swallow
it. This is due to the tannins it contains. If this description sounds too
abstract, simply try out various oils to find the best, using the various
quality seals as a guide.
But merrily drizzling your olive oil into the pan for frying is not
such a good idea as heat can cause a lot of damage. Hotplates are
great for frying up steaks or eggs, but they are not good for oily fatty
acids, which can be chemically altered by heat. Cooking oil or solid
fats such as butter or hydrogenated coconut oil should be used for
frying. They may be full of the much-frowned-upon saturated fats,
but they are much more stable when exposed to heat.
Fine oils are not only sensitive to heat, they also tend to capture
free radicals from the air. Free radicals do a lot of damage to our
bodies because they don’t actually like being free, much preferring to
bond with other substances. They can latch onto almost anything—
blood vessels, facial skin, or nerve cells—causing inflammation of
the blood vessels (vasculitis), aging of the skin, or nerve disease.
That’s why you should always close the bottle or container of olive oil
carefully after use and keep it in the fridge.
The animal fats found in meat, milk, and eggs contain far more
arachidonic acid than vegetable fats. Arachidonic acid is converted
in our body into neurotransmitters involved in the sensation of pain.
Oils such as rapeseed (canola), linseed, or hempseed oil, on the
other hand, contain more of the anti-inflammatory substance alphalinolenic acid, while olive oil contains a substance with a similar
effect called oleocanthal. These fats work in a similar way to
ibuprofen or aspirin, but in much smaller doses. So, although they
are no help if you have an acute headache, using these oils regularly
can help those who suffer from inflammatory disease, regular
headaches, or menstrual pain. Sometimes, pain levels can be
reduced somewhat simply by taking care to eat more vegetable fat
than animal fat.
However, olive oil should not be seen as a panacea for all skin
and hair conditions. Dermatological studies have shown that pure
olive oil can even irritate the skin slightly, and that using olive oil as a
hair treatment leaves hair so oily that the amount of washing
required to remove the oil negates any possible beneficial effects.
It is easy to overdo it with fats inside our bodies, too. Large
amounts—of either good or bad fat—are simply too much for the
body to deal with. It’s comparable to smearing too much moisturizer
on your face. Nutritional physiologists recommend we get between
25 and a maximum of 30 percent of our daily energy requirement
from fat. That works out at an average of 2 to 2½ ounces (55 to 66
grams) of fat a day. Larger, more athletic types may consume a little
more; smaller, more sedentary types should try to consume a little
less. This means if you eat just one Big Mac, you will have
conveniently covered half your daily requirement of fat—the only
question is, with what kind of fat? A sweet onion chicken teriyaki
sandwich from the fast-food chain Subway contains less than 1/6 of
an ounce of fat (only 4.5 grams). How you consume the other 2
ounces (53 grams) is then entirely up to you.
Having examined carbohydrates and fats, there is just one more
nutritional building block to consider. It is probably the least familiar:
amino acids. It seems strange to imagine, but both tofu, with its
neutral-to-nutty taste, and salty, savory meat are made up of lots of
tiny acids. As with carbohydrates, these tiny building blocks are
linked in chains. This is what gives them their different taste and a
different name—proteins. Digestive enzymes break down these
chains in the small intestine and then the gut wall nabs the valuable
components. There are twenty of these amino acids and an infinite
variety of ways they can be linked to form proteins. We humans use
them to build many substances, not least of which is our DNA, the
genetic material contained in every new cell we produce every day.
The same is true of other living things, both plants and animals. That
explains why everything nature produces that we can eat contains
protein.
However, maintaining a healthy meat-free diet that does not lead
to nutritional deficiencies is more difficult than most people think.
Plants construct different proteins than animals, and they often use
so little of a given amino acid that the proteins they produce are
known as incomplete. When our body tries to use these to make the
amino acids it needs, it can continue to build the chain only until one
of the amino acids runs out. Half-finished proteins are then simply
broken down again, and we excrete the tiny acids in our urine or
recycle them in our body. Beans lack the amino acid methionine; rice
and wheat (and its derivative meat substitute, seitan) lack lysine; and
sweetcorn is, in fact, deficient in two amino acids: lysine and
tryptophan. But this does not spell the final triumph of the meat
eaters over the meat-avoiders. Vegetarians and vegans simply have
to be cleverer in combining their foods.
Beans may be lacking in methionine, but they are packed with
lysine. A wheat tortilla with refried beans and a yummy filling will
provide all the amino acids the body needs for healthy protein
production. Vegetarians who eat cheese and eggs can compensate
for incomplete proteins that way. For centuries in many countries
around the world, people have intuitively eaten meals made up of
foodstuffs that complement each other: rice and beans, pasta with
cheese, pita bread and hummus, or peanut butter on toast. In theory,
combining does not even have to take place within one meal. It is
enough to take in the right combination over the course of a day.
(Thinking about these combinations can often inspire even the most
uninventive of cooks when they are trying to decide what to make for
dinner.) There are plants that do contain all the necessary amino
acids in the necessary quantities. Two of these are soy and quinoa,
but others include amaranth, spirulina, buckwheat, and chia seeds.
Tofu has a well-deserved reputation as an alternative to meat—with
the caveat that increasing numbers of people are developing allergic
reactions to it.
Allergies and Intolerances
ONE THEORY ABOUT the origin of allergies begins with the digestive
processes in the small intestine. If we fail to break down a protein
into its constituent amino acids, tiny bits of it will remain. Under
normal circumstances, those tiny particles simply don’t make it into
our bloodstream and there is no problem. However, hidden power
often lies in the most inconspicuous places—in this case, in the
lymphatic system. Those tiny particles can enter the lymphatic
system, embedded in fat droplets, and once there, they attract the
attention of ever-vigilant immune cells. When the immune cells
discover a tiny particle of peanut in the lymphatic fluid, for example,
they naturally attack it as a foreign body.
The next time the immune cells encounter a peanut particle, they
are better prepared to deal with it and can attack it more
aggressively. And so it goes on, until we reach the stage where just
putting a peanut in our mouth causes our immune cells to whip out
the big guns straightaway. The result is increasingly severe allergic
reactions, such as extreme swelling of the face and tongue. This
explanation applies to allergies caused by foods that are both fatty
and rich in protein, such as milk, eggs, and, most commonly,
peanuts. There is a simple reason almost no one is allergic to greasy
bacon. We are made of meat ourselves, and so we generally have
few problems digesting it.
Celiac Disease and Gluten Sensitivity
in the small intestine are not limited to fats.
Allergens such as prawns, pollen, or gluten, for example, are not, in
themselves, fat-bombs, and people who eat a fatty diet do not
necessarily suffer from more allergies than others. Another theory
about how allergies develop is this: the wall of our gut can become
temporarily more porous, allowing food remnants to enter the tissue
of the gut and the bloodstream. This is the theory under most
scrutiny from researchers who are interested in gluten—a protein
found in wheat and related grains.
Grains do not like us to eat them. What plants really want is to
reproduce—and then along we come and eat their children. Instead
of creating an emotional scene, plants respond by making their
seeds slightly poisonous. That sounds much more drastic than it is—
neither side is going to lose much sleep over a few guzzled wheat
grains. The arrangement means humans and plants both survive
well enough. But, the more danger a plant senses, the more
poisonous it will make its seeds. Wheat, in particular, is such a
worrier because it has only a very short window of opportunity for its
seeds to grow and carry on the family line. With such a tight
schedule, nothing must be allowed to go wrong. In insects, gluten
has the effect of inhibiting an important digestive enzyme. A greedy
grasshopper might be put off by a little stomachache after eating too
much wheat, and that is to the benefit of both plant and animal.
In humans, gluten can pass into the cells of the gut in a partially
undigested state. There, it can slacken the connections between
individual cells. This allows wheat proteins to enter areas they have
no business being in. That, in turn, raises the alarm in our immune
system. One person in a hundred has a genetic intolerance to gluten
(celiac disease), but a considerably higher proportion suffer from
gluten sensitivity.
ALLERGIES THAT DEVELOP
In patients with celiac disease, eating wheat can cause serious
infections or damage to the villi of the gut wall; it can also damage
the nervous system. Celiac disease can cause diarrhea and failure
to thrive in children, who may show reduced growth or winter pallor.
The tricky thing about celiac disease is that it can appear in more or
less pronounced forms. Those with more subtle forms may live with
the symptoms for years without realizing it. They may have the
occasional stomachache, or their doctor might discover signs of
anemia during routine blood tests. Currently, the most effective
treatment is a lifelong gluten-free diet.
Gluten sensitivity, by contrast, is not a sentence to a life of gluten
avoidance. Those with this condition can eat wheat without risking
serious damage to their small intestine, but they should enjoy wheat
products in moderation—a little bit like our friend the greedy
grasshopper. Many people notice their sensitivity when they swear
off gluten for a week or two and see an improvement in their general
well-being. Suddenly, their digestive problems or flatulence clear up,
or they have fewer headaches or less painful joints. Some people
find that their powers of concentration improve, or that they are less
plagued by tiredness or fatigue. Researchers began exploring gluten
sensitivity in detail only recently. Currently, the diagnostic picture can
be summarized as follows. Symptoms improve when a gluten-free
diet is introduced, although tests for celiac disease show negative.
The villi are not inflamed or damaged, but eating too much bread still
appears to have an unpleasant effect on the immune system.
The gut can also become porous for a short time after a course of
antibiotics, after a heavy bout of drinking alcohol, or as a result of
stress. Sensitivity to gluten resulting from these temporary causes
can sometimes look the same as the symptoms of true gluten
intolerance. In such cases, it can be helpful to avoid gluten for a
time. A thorough medical examination and the detection of certain
molecules on the surface of the blood corpuscles are important for a
definitive diagnosis. Alongside the familiar blood groups A, B, AB,
and O, there are many other indicators for categorizing human
blood, including what doctors call DQ markers. Those who do not
belong to group DQ2 or DQ8 are extremely unlikely to have celiac
disease.
Lactose Intolerance and
Fructose Intolerance
is not an allergy or a real intolerance at all, but
a deficiency. But it, too, results from a failure to break down certain
nutrients completely into their component parts. Lactose is found in
milk. It is derived from two sugar molecules that are linked together
by chemical bonds. The body requires a digestive enzyme to break
that bond, but, unlike other enzymes, this one does not come from
the papilla. The cells of the small intestine secrete it themselves on
the tips of their tiny little villi. Lactose breaks down when it comes
into contact with the enzyme on the gut wall, and the resulting single
sugars can then be absorbed. If the enzyme is missing, similar
problems arise to those caused by gluten intolerance or gluten
sensitivity, including bellyache, diarrhea, and flatulence. Unlike in
celiac disease, however, no undigested lactose particles pass
through the gut wall. They simply move on down the line, into the
large intestine, where they become food for the gas-producing
bacteria there. Consider the resulting flatulence and other
unpleasant symptoms as votes of thanks from extremely satisfied,
overfed microbes. Although the results can be unpleasant, lactose
intolerance is far less harmful to health than undiagnosed celiac
disease.
LACTOSE INTOLERANCE
Every human being has the genes needed to digest lactose. In
extremely rare cases, problems with lactose digestion can occur
from birth. Such newborns are unable to digest their mother’s milk,
and drinking it causes severe diarrhea. In 75 percent of the world’s
population, the gene for digesting lactose slowly begins to switch off
as they get older. This is not surprising, as by then we are no longer
reliant on our mothers’ milk, or formula milk, to nourish us. Outside of
Western Europe, Australia, and the United States, adults who are
tolerant to dairy products are a rarity. Even in our parts of the world,
supermarket shelves are increasingly full of lactose-free products.
Recent estimates say about 25 percent of people in the United
States lose their ability to break down lactose after weaning. The
older a person, the greater the probability that she will be unable to
break down lactose—although very few sixty-year-olds would dream
of blaming their daily glass of milk or that delicious dollop of cream
for a bloated stomach or a little bit of diarrhea.
However, lactose intolerance does not mean you must cut out
milk products altogether. Most people have enough lactose-splitting
enzymes in their gut. It is just that their activity is somewhat reduced
—down to about 10 to 15 percent of their initial level, let’s say. So if
you notice your stomach feels better when you don’t drink that glass
of milk, you can simply use trial and error to find out just how much
your body can deal with, and how much dairy produce it takes to
make the problems come back. A nibble of cheese or a splash of
milk in your tea or coffee will usually be fine, as will the occasional
milk pudding or cream filling in your cake.
A common children’s counting rhyme in Germany, comparable to
the “eeny, meeny, miny, moe” of the English-speaking world,
translates as “Ate cherries, drank water, got tummy ache, went to
hospital!” The most common food intolerance in the Western
hemisphere is trouble digesting the fruit sugar fructose, with about
40 percent of the population affected. Fructose intolerance can be
the result of a severe hereditary inability to metabolize fruit sugar,
which causes patients’ digestive systems to react to even the tiniest
amounts of the substance. But most people affected by fructose
intolerance actually have a condition more accurately described as
fructose malabsorption, and they experience problems only when
they are exposed to large amounts of the sugar. When fructose is
described on food packages as “fruit sugar,” consumers often
assume it is a healthier, more natural option. This explains why food
manufacturers choose to sweeten their products with pure fructose,
and consequently why our digestive system is exposed to more of
this type of sugar than ever before.
An apple a day would not present a problem to most people who
are fructose intolerant if it weren’t for the fact that the ketchup on
their fries, the sweetening agent in their breakfast yogurt, and the
can of soup they heated up for lunch, all contain added fructose.
Some types of tomato are specially bred to contain large amounts of
this sugar. Furthermore, globalization and air transport mean that we
are now exposed to a previously unheard-of overabundance of fruit.
Pineapples from the tropics nestle on our supermarket shelves in the
middle of winter, next to fresh strawberries from Mexico, and some
dried figs from Morocco. So, what we label a food intolerance may in
fact be nothing more than the reaction of a healthy body as it tries to
adapt within a single generation to a food situation that was
completely unknown during the millions of years of our evolution.
The mechanism behind fructose intolerance is different once
again from that involved in the digestion of gluten or lactose. The
cells of people with hereditary fructose intolerance contain fewer
fructose-processing enzymes. That means fructose may gather in
their cells, where it can interfere with other processes. Fructose
intolerance that appears later in life is thought to be caused by a
reduced ability of the gut to absorb fruit sugars. Such patients often
have fewer transporters (called GLUT5 transporters) in their gut wall.
When they ingest even a small amount of fruit sugar—for example,
by eating a pear—their limited transporters are overwhelmed and, as
with lactose intolerance, the sugar from the pear ends up feeding the
flora of the large intestine. However, some researchers question
whether a lack of sufficient transporters really is the cause of this
problem, since even those without the condition pass some of the
fructose they eat into the large intestine undigested (especially after
eating very large amounts of it). The problems experienced by such
people may be due to an imbalance in their gut flora. When they eat
a pear, the extra sugar is gobbled up by the gut bacteria squad,
which then produces rather unpleasant symptoms. Of course, the
more ketchup, canned soup, or sweetened yogurt they have eaten,
the worse their troubles will be.
Fructose intolerance can also affect our mood. Sugar helps the
body absorb many other nutrients into the bloodstream. The amino
acid tryptophan likes to latch on to fructose during digestion, for
example. When there is so much fructose in our gut that most of it
cannot be absorbed into the blood and we lose that sugar, we also
lose the tryptophan attached to it. Tryptophan, for its part, is needed
by the body to produce serotonin—a neurotransmitter that gained
fame as the happiness hormone after it was discovered that a lack of
it can cause depression. Thus, a long-unrecognized fructose
intolerance can lead to depressive disorders. General practitioners
and family doctors are only now beginning to include this knowledge
in their diagnostic toolkit.
This raises the question whether a diet that includes too much
fructose can also affect our mood, even in the absence of an
intolerance. For more than 50 percent of people, eating 2 ounces (50
grams) of fructose or more per day (equivalent to five pears, eight
bananas, or about six apples) will overtax their natural transporters.
Eating more than that can lead to health problems such as diarrhea,
stomachaches, and flatulence, and, over longer periods, to
depressive disorders. The fructose intake of the average American is
currently close to 3 ounces (80 grams) a day. Our parents’
generation, consuming just honey on their toast, far fewer processed
foods, and a normal amount of fruit, took in no more than ½ to 1
ounce (only around 16 to 24 grams) a day.
Serotonin not only puts us in a good mood, it is also responsible
for making us feel pleasantly full after a meal. Snack attacks or
constant grazing on snacks may be a side effect of fructose
intolerance if they are accompanied by other symptoms, such as
stomachaches. This is also an interesting hint for all diet-conscious
salad eaters, since many salad dressings found on our supermarket
shelves or at fast-food outlets now contain fructose-glucose syrup
(often known as high-fructose corn syrup). Studies have shown that
this syrup can suppress leptin, the hormone that makes us feel full,
even in people who are not fructose intolerant. A salad containing
the same amount of calories but with a homemade vinaigrette or
yogurt dressing will keep you feeling full for longer.
Like everything else in the world, food production is constantly
changing. Sometimes those changes are good for us and sometimes
they are bad. Curing was once the state-of-the-art way of ensuring
people were not poisoned by eating rotten meat. For centuries, it
was common practice to cure meats and sausages with large
quantities of nitrite salts. This gives them a pinkish red, fresh color,
and explains why products such as ham, salami, tinned pork, or
gammon do not turn the same brown-gray color in the frying pan as
an unprocessed chop or steak.
Use of nitrites for food preservation has been highly regulated
since the 1980s, due to concerns about possible negative effects on
human health. In the United States, sausage and cold meat products
must contain no more than 156 parts per million of nitrite salt,
approximately one-fifth of the level allowed twenty-five years ago.
Rates of stomach cancer have fallen considerably since these
regulations were introduced. This shows that what had once been a
very sensible meat-preserving technique was in drastic need of
correction. Today, canny butchers mix large amounts of vitamin C
with small amounts of nitrite to cure their meats safely.
A similar modern reassessment of ancient practices may be in
order in the case of wheat, milk, and fructose. It is good to include
these foodstuffs in our diet, since they contain valuable nutrients, but
it may be time to reassess the quantities we consume. While our
hunter-gatherer ancestors ate up to five hundred different local roots,
herbs, and other plants in a year, a typical modern diet includes
seventeen different agricultural plant crops at most. It is not
surprising that our gut has a few problems with a dietary change of
that scale.
Digestive issues divide society into two groups: those who worry
about their health and pay great attention to their nutrition, and those
who get annoyed by the fact that they can no longer invite a group of
friends round for a meal without having to go shopping at the
pharmacy. Both groups are right. Many people err on the side of
caution after hearing from their doctor about a food intolerance and
then noticing that they do feel better if they avoid certain foods. They
might decide to cut out fruit, wheat, or dairy products, and then often
act as if they were poisonous. In fact, most people react to excessive
amounts of these foodstuffs without being genetically intolerant to
them. Most have enough enzymes to process a small portion of
creamy sauce, the occasional pretzel, or a fruit pudding.
However, this does not mean that real intolerances should be
ignored. We do not need to swallow every new development in our
food culture blindly. Wheat products for breakfast, lunch, and dinner,
fructose in practically all processed foods, or milk products long after
weaning—it is not surprising that our bodies sometimes rebel.
Symptoms like regular stomachaches, repeated bouts of diarrhea, or
severe fatigue do not occur for no reason, and nobody should be
expected to just accept them as “one of those things.” Even if your
doctor has ruled out celiac disease or hereditary fructose
intolerance, nobody can deny you the right to avoid certain foods if
you notice that doing so improves your general well-being.
Apart from this general overconsumption, antibiotics, high stress
levels, or gastrointestinal infections, for example, can also trigger
temporary sensitivities to certain foods. When the body has returned
to a healthy equilibrium, even a sensitive gut can usually sort itself
out. Then there is no need to impose a lifelong ban on certain
products, but simply to make sure you consume them in quantities
your system can easily cope with.
A FEW FACTS
ABOUT FECES
COMPONENTS
COLOR
CONSISTENCY
GENTLE READER, it is now time to get down to the nitty-gritty. So, hitch up your
suspenders, push your glasses up the bridge of your nose, and take a good gulp of your
tea. While maintaining a safe distance, we must now take a closer look at the mysteries of
number twos!
COMPONENTS
Many people believe feces are made up mainly of what they have eaten. That is not the
case.
Feces are three-quarters water. We lose around 3½ ounces (100 milliliters) of fluid a
day. During a passage through our digestive system, some 10 US quarts (9.8 liters) are
reabsorbed. What we deliver into the toilet bowl is the result of an absolute maximum level
of efficiency. Whatever fluid is left in the feces belongs there. This optimum water content
makes our feces soft enough to ensure our metabolic waste products can be transported
out of our bodies safely.
A third of the solid components are bacteria. They are gut flora that have ended their
careers in the digestive business and are ready to retire from the workplace.
Another third is made up of indigestible vegetable fiber. The more fruit and vegetables
you eat, the more feces you excrete per bowel movement. Increasing the proportion of that
food group in the diet can raise the weight of a bowel movement from the average 3½ to 7
ounces (100 to 200 grams) to as much as 17 or 18 ounces (500 grams) per day.
The remaining third is a mixed bag. It is made up of substances that the body wants to
get rid of—such as the remains of medicines, food coloring, or cholesterol.
COLOR
The natural color of human feces ranges from brown to yellowish-brown—even when we
have not eaten anything of this color. The same is true of our urine—it always tends toward
yellow. This is due to a very important product that we manufacture fresh every day: blood.
Our bodies create 2.4 million new blood corpuscles a day. But the same number are broken
down every day, too. In that process, the red pigment they contain is first turned green, then
yellow. You can see the same process in the various stages of a bruise on your skin. A
small portion of this yellow pigment is excreted in your urine.
Most of it, though, passes through the liver and into the gut. There, bacteria change its
color once again—this time turning it brown. Examining the color of feces can provide a
useful insight into the goings-on of our gut.
LIGHT BROWN TO YELLOW: This color can be the result of the harmless disorder called
Gilbert’s syndrome (or Gilbert-Meulengracht syndrome). In this condition, one of the
enzymes involved in the breakdown of blood works at only 30 percent of its normal
efficiency. This means less pigment finds its way into the gut. Affecting around 8 percent of
the world’s population, Gilbert’s syndrome is relatively common. This enzyme defect is not
harmful, causing barely any problems for those who have it. The only side effect is a
reduced tolerance for acetaminophen, which should be avoided by those with Gilbert’s
syndrome.
Another possible cause of yellowish feces is problems with the bacteria in the gut. If they
are not working as they should, the familiar brown pigment will not be produced. Antibiotics
or diarrhea can cause such an alteration in fecal color.
LIGHT BROWN TO GRAY: If the connection between the liver and the gut is blocked by a
kink in the tubes or by pressure (usually behind the gall bladder), no blood pigment can
make it into the feces. Blocked connections are never a good thing, and those who notice a
gray tint to their feces should consult their doctor.
BLACK OR RED: Congealed blood is black and fresh blood is red. In this case, the color is
not due to the pigment that can be turned brown by bacteria, but to the presence of entire
blood corpuscles. For those with hemorrhoids, a small amount of bright red blood in the
stool is no reason to worry. However, anything darker in color than fresh, bright red blood
should be checked by a doctor—unless you have been eating large amounts of beetroot.
CONSISTENCY
The Bristol stool scale was first published in 1997, so it is not very old if you consider the
millions of years that feces have existed. The scale classifies the consistency of feces into
seven groups. A chart like this can be a useful tool, since most people are reluctant to talk
about the appearance of their bowel movements. That’s perfectly natural. There are some
aspects of private life we prefer not to rub other people’s noses in! But such a reticence to
talk about what we find in the toilet bowl means that people with unhealthy looking feces are
often unaware of it. They think everybody’s business looks like their own. A healthy
digestive system, producing feces with the optimum water content, will produce types 3 or 4.
The other types are less than ideal. If they do appear, a good doctor should be able to find
out whether your loose stool or constipation is the result of a food intolerance, for example.
The chart was developed by Dr. Ken Heaton at the University of Bristol in the United
Kingdom.
TYPE 1
Separate hard lumps, like nuts (hard to pass)
TYPE 2
Sausage-shaped, but lumpy
TYPE 3
Like a sausage but with cracks on its surface
TYPE 4
Like a sausage or snake, smooth and soft (author’s note: like toothpaste)
TYPE 5
Soft blobs with clear-cut edges (passed easily)
TYPE 6
Fluffy pieces with ragged edges, a mushy stool
TYPE 7
Watery, no solid pieces, entirely liquid
The type a person’s feces belong to can be an indication of how long indigestible
particles take to pass through their gut. According to this, in Type 1 digestive remains take
around one hundred hours to pass through the system (constipation). In Type 7, they pass
through in just ten hours (diarrhea). Type 4 is considered the ideal, because it has the
optimum ratio between fluid and solid content. Those who find types 3 or 4 in the toilet bowl
may also want to observe how quickly their feces sink in water. Ideally, they should not
plummet straight to the bottom, as this would indicate the possibility that they still contain
nutrients that have not been digested properly. Feces that sink slowly contain bubbles of
gas that keep them afloat in water. These gas bubbles are produced by gut bacteria that
mostly perform useful services. So this is a good sign, as long as it is not accompanied by
flatulence.
THESE HAVE BEEN a few selected facts about feces, gentle reader. You can now loosen
your suspenders and let your glasses slide back down your nose to where they are most
comfortable. Here endeth the first chapter of the story of the gut and its goings-on. We now
turn to an electrifying topic: the nerves.
(PART TWO)
THE NERVOUS
SYSTEM
OF THE GUT
THERE ARE PLACES where the unconscious and the conscious
meet. When you are sitting at home, eating your lunch, you may be
unaware that your next-door neighbor is just a short distance away,
beyond the dividing wall, chomping away on his lunch, too. You
might hear the faint creak of his floorboards and suddenly, your
awareness reaches out beyond your own four walls. Similarly, there
are areas of our own body we are simply unaware of. You don’t feel
your organs working away all day long. When you eat a piece of
cake, you taste it while it is still in your mouth, and you are also
conscious of the beginning of its journey as it passes down your
throat after you swallow it. But then, as if by magic, the cake is gone!
From then on, what we eat disappears into the realm of what
scientists call smooth muscle.
Smooth muscle is not under our conscious control. Under the
microscope, it looks very different from the tissue of the muscles we
can control consciously, such as the biceps. We can flex and relax
the muscles in our upper arms at will. Such muscles are made up of
the tiniest little fibers, lined up so neatly they look as if they were
drawn using a ruler.
The microscopic structure of smooth muscle resembles an
organic network, and it moves in mellifluous waves. Our blood
vessels are surrounded by smooth muscle tissue, which explains
why we blush when we are embarrassed. Smooth muscle tissue
slackens in response to emotions such as embarrassment, causing
the blood capillaries in the skin of the face to dilate. In many people,
stress has the opposite effect, causing the muscles surrounding the
blood vessels to contract, restricting the flow of blood. This can lead
to high blood pressure.
The gut is cosseted by no fewer than three coats of smooth
muscle tissue. This makes it incredibly supple and able to execute
different choreographies in different places. The choreographer
directing these muscles is the gut’s own (enteric) nervous system.
The enteric nervous system controls all processes that take place in
the digestive tract, and it is extraordinarily autonomous. If the
connection between the enteric nervous system and the brain is
severed, the digestive tract carries blithely on as if nothing has
happened. This property is unique to the enteric nervous system and
is found nowhere else in the human body—without directions from
our brain, our legs would be lame and our lungs would no longer be
able to breathe. It is a shame that we are oblivious to the workings of
these independent-minded nerve fibers. Burping or breaking wind
might sound a bit gross, but the movements involved are as delicate
and complex as those of a ballerina.
How Our Organs Transport Food
ALLOW ME TO take you on a journey. Let us accompany that piece of
cake on its travels in the realm of smooth muscle.
Eyes
bouncing off the piece of cake hit the optic nerves
at the back of the eyes, generating a nerve impulse. This first
impression travels right through the brain to the visual cortex at the
back, just below where a high ponytail would be. There, the brain
interprets the nerve impulses to form an image. It is not until that
happens that we really see the piece of cake. This delicious news is
then passed on to the systems that control salivation, with mouthwatering results. Similarly, the mere sight of a yummy treat also
causes the stomach to produce some digestive juices in anticipation.
PARTICLES OF LIGHT
Nose
your finger up your nose, you will notice that the cavity
continues upward far beyond the reach of your finger. This is where
the olfactory nerves are, which are responsible for smelling. They
are coated in a protective layer of mucus, so anything we smell must
IF YOU STICK
first be dissolved in that slimy substance if it is to get through to the
nerves.
Olfactory nerves are specialists. There are specific receptors for
a large range of individual smells. Some spend years hanging
around up your nose, waiting for their chance to shine. When that
single, long-awaited lily-of-the-valley scent molecule finally attaches
itself, the receptor proudly calls out “lily-of-the-valley!” to the brain.
Then it might be idle again for the next couple of years. (Incidentally,
although we are equipped with a large number of olfactory cells,
dogs have inconceivably more.)
For us to smell it, molecules from the piece of cake first have to
drift into the air, to be sucked in through our nostrils as we breathe.
They may be aromatic molecules of vanilla, minute plastic molecules
from cheap party forks, or evaporating alcohol fragrances from the
cake’s rum filling. Our olfactory organ is a royal taster with a
thorough knowledge of chemistry. The closer we bring the cakeladen fork to our cake-hole, the more detached cake molecules
stream into our nose. If we detect tiny traces of alcohol as the cake
covers the last small gap between our fork and our mouth, we may
back our arm up in suspicion to allow our eyes to inspect the cake
again, just to check whether it is supposed to contain alcohol or
whether the fruit in it has started to rot. With all checks passed, it’s
mouth open, fork in, and let the ballet begin.
Mouth
a place of superlatives. The most powerful muscles in
our body are the jaw muscles; the body’s most flexible striated (not
smooth) muscle is the tongue. Working together, they are not only
incredible crunchers, they are also nimble manipulators. Another
THE MOUTH IS
candidate for the record books is tooth enamel. Tooth enamel is the
hardest substance produced by the human body. And it needs to be,
since our jaws can exert a pressure of up to 180 pounds (80 kilos)
on each of our molars—or approximately the weight of a grown man!
When we encounter something hard in our food, we pound it with
almost the equivalent force of an entire football team jumping up and
down on it before we swallow it. All that power is not necessary to
deal with a piece of cake—just a few girls in tutus and ballet slippers
will suffice.
The tongue plays an important part in mastication. It acts like a
football coach, gathering any bits of cake that may be hiding from the
chewing action and guiding them back into the game. When the
mouthful of cake is sufficiently mushy, it is ready for swallowing. The
tongue rounds up about half an ounce (20 milliliters) of cake mush
and presses it against the palate, the stage curtain of the
esophagus. It works like a light switch: when the tongue presses
against it, the swallowing reflex starts automatically. We close our
mouth, since breathing must stop for swallowing to take place. The
ball of cake mush—known medically as the bolus—now makes its
way toward the pharyngeal area, and it’s time for the dancers to
enter the stage and the show to start.
Pharynx
THE VELUM (OR
soft palate) and the superior pharyngeal constrictor
muscle are the two formations responsible for officially closing the
connections to the nose. This movement is so powerful that it can be
heard down the corridor and round the corner—that popping sound
in the ear that often accompanies a powerful swallow. The vocal
cords are silenced and have to be closed. The epiglottis rises
majestically, like an orchestra conductor (you can feel it when you
place a hand on your neck), the entire base of the mouth is lowered,
and a powerful wave pushes the bit of cake into the esophagus,
amid tumultuous applause from the salivary system.
Esophagus
takes five to ten seconds to reach this stage. When
we swallow, our esophagus executes a kind of stadium-style wave.
On the arrival of the bolus, the esophagus widens to let it pass,
closing again behind it. This prevents anything from slipping back up
the wrong way.
This process is so automatic that it even works when the owner
of the esophagus is standing on her head. Our piece of cake
meanders in this way—oblivious to gravity—gracefully through the
upper body. Break dancers would call this move The Snake or The
Worm; doctors prefer to call it propulsive peristalsis. The top third of
the esophagus is surrounded by striated muscle—that is why we are
still aware of the cake passing through that part of the gullet. The
unconscious inner world begins at the level of that small hollow you
can feel at the top of your breastbone. From there on, the esophagus
is made of smooth muscle.
The esophagus is sealed at the bottom end by a ring-shaped
sphincter muscle. Taking its cue from the peristaltic motion above,
that muscle relaxes for eight frolicsome seconds. This opens the
way, allowing the piece of cake to plop unhindered into the stomach.
The muscle then closes again, and normal breathing service
resumes up in the pharynx.
The journey from mouth to stomach is the first act of the
performance. It requires maximum concentration and good
THE CAKE BOLUS
teamwork. The conscious peripheral nervous system and the
unconscious autonomous nervous system must work together in
perfect harmony. This cooperation must be well rehearsed. We begin
practicing swallowing as unborn babies in the womb. We swallow up
to one pint (half a liter) of amniotic fluid a day during this test phase.
If something goes wrong at this stage, no harm is done. Since we
are completely surrounded by liquid, and our lungs are full of it
anyway, we are unable to choke in the normal sense.
As adults, we swallow somewhere between six hundred and two
thousand times a day. And each act of swallowing involves more
than twenty pairs of muscles. Despite this frequency and complexity,
things rarely go wrong. In old age, we are more prone to choking.
The muscles that coordinate the process may no longer work quite
so precisely. The superior pharyngeal constrictor muscle might not
be quite the strict timekeeper it was in its youth, or the epiglottal
conductor may need the aid of a stick to climb up to the podium.
Pounding someone on the back when they are choking is a wellmeant gesture, but it does little more than startle the aging
pharyngeal team unnecessarily. A better strategy is to seek out a
speech therapist to help you whip your swallowing squad into good
shape before choking attacks become too frequent.
Stomach
IS much more of a mover than many people think.
Shortly before our piece of cake plops in, it relaxes to accommodate
it—and it can keep relaxing and stretching for as long as food keeps
arriving. It will make room for as much as we can guzzle. Two
THE STOMACH
pounds (one kilo) of cake about the size of a carton of milk will easily
fit into this stretchable swing hammock of a stomach. Emotions like
fear or stress can reduce the ability of the smooth muscle to stretch,
making us feel full—or even nauseous—after eating just a small
portion of food.
Once the cake arrives, the walls of the stomach speed up their
movements, just like the legs of a person accelerating into a run,
then—bam!—the food gets a big push. Describing an elegant arc, it
is lobbed against the stomach wall, where it bounces off and plops
back down. Medics call this process retropulsion. Older brothers and
sisters call it “let’s see how far I can throw you.” This acceleration,
push, and plop process is what causes the gurgling sound you can
hear if you press your ear against the top of someone’s belly (in the
little triangle where the ribs meet). When the stomach starts merrily
swinging to and fro, the rest of the digestive tract is galvanized into
action as well. This leads the gut to move its contents on down the
line, making room for the next batch. That’s why we often feel the
urge to seek out the toilet soon after enjoying a large meal.
A piece of cake can really get things going in the belly region.
The stomach will churn it for about two hours, grinding the mouthfuls
into tiny particles, most of them less than one-twelfth of an inch
(about 2 millimeters) in size. Scraps of that size are no longer lobbed
against the stomach wall, but slip through a little hole at the end of
the stomach. This hole is the next sphincter—the doorman who
guards the stomach’s exit and the entrance to the small intestine.
Simple carbohydrates such as sponge cake, rice, or pasta make
it through to the small intestine pretty quickly. There, they are
digested and rapidly cause an increase in the levels of sugar in our
blood. The doorman detains proteins and fats in the stomach for
considerably longer. A piece of steak may easily be churned about
for six hours before all of it has disappeared into the small intestine.
This explains why we often fancy a sweet dessert after eating meat
or fatty, fried foods. Our blood sugar levels are impatient and want to
rise quickly, and dessert provides a quick blood sugar fix. Meals rich
in carbohydrates may perk us up more quickly, but they do not keep
us feeling full for as long as meaty or fatty meals.
Small Intestine
reach the small intestine, the real process of
digestion begins. As it passes through this tube, the motley cake
mush will almost completely disappear into its walls—a bit like Harry
Potter on Platform 9¾. The small intestine pluckily pounces on the
piece of cake. It squeezes it, hashes it up from all sides, wiggles its
villi in what we might now call the cake chyme, and when it is
thoroughly mixed, moves it on down the digestive line. Under the
microscope we can see that even the microvilli help it along! They
move up and down like tiny trampling feet. Everything is in motion.
Whatever our small intestine does, it always obeys one basic
rule: onward, ever onward! This is achieved by the peristaltic reflex.
The man who first discovered this mechanism did so by isolating a
piece of gut and blowing air into it through a small tube—and the
friendly gut blew right back. This is why many doctors recommend a
high-fiber diet to encourage digestion: indigestible fiber presses
against the gut wall, which becomes intrigued and presses back.
These gut gymnastics speed up the passage of food through the
system and make sure the gut remains supple.
If our cake chyme were to listen carefully, it might hear a “heave!”
The wall of the small intestine contains a particularly large number of
pacemaker cells, which emit tiny bioelectric pulses. For the muscles
of the gut, that is as if someone were to shout “heave!” and then
again “heave!” In this way, the muscle is prevented from drifting off
WHEN THE MINI-MORSELS
course, and it “heaves” back into place like a clubber on the dance
floor responding to the beat. This keeps the piece of cake, or what’s
left of it, moving unerringly onward.
The small intestine is the hardest-working part of our digestive
tract, and it is very diligent about doing its job. There is only one
unequivocal exceptional case when it does not see a digestive
project through to the end: when we throw up. The small intestine is
quite pragmatic when we need to vomit. It does not invest work in
something that will not do us any good. It simply sends such stuff
straight back by return mail.
Apart from a few remnants, our piece of cake has now
disappeared entirely into the bloodstream. We could now follow
those stragglers as they pass into the large intestine, but then we
would miss a mysterious and oft-misunderstood creature that we can
hear but not see. So let’s stay a little while longer and get acquainted
with it.
After digestion, only a few rough leftovers remain in the stomach
and small intestine—an unchewed kernel of corn, tablets coated to
stop them dissolving in gastric juices, surviving bacteria from the
food we have eaten, or a piece of chewing gum swallowed by
mistake, for example. Now, the small intestine is a stickler for
cleanliness. It is one of those types who clean up the kitchen right
after a meal. If you were to pay your small intestine a visit just two
hours after it has finished digesting something, you would find
everything spick and span, with barely a whiff of what went on there
a short time ago.
An hour after the small intestine has digested something, it
begins the cleanup process. The scientific name for this process is
“migrating motor complex.” When it kicks in, the stomach doorman is
kind enough to open the gates again to allow these leftovers to be
herded into the small intestine. It then moves them along with a
wave powerful enough to sweep everything along with it. When
observed with a camera, this looks so cute that even sober-minded
scientists can’t help but nickname the migrating motor complex the
little “housekeeper.”
Everyone has heard their little housekeeper at work. It is the
rumbling belly, which, contrary to popular belief, does not come
mainly from the stomach, but from the small intestine. Our bellies
don’t rumble when we’re hungry, but when there is a long enough
break between meals to finally get some cleaning done! When the
stomach and the small intestine are both empty, the coast is clear for
the housekeeper to do its work. If the stomach is involved in the
lengthy process of grinding down a steak, the housekeeper just has
to be patient. Only after six hours of churning in the stomach and
around five hours of digesting in the small intestine is the steak
safely gone and the housekeeper can start clearing up. We don’t
necessarily always hear the housekeeper at work. It depends on
how much air has found its way into the stomach and the small
intestine. If we eat something before the cleanup is finished, the
housekeeper immediately stops working and returns to waiting
mode. Food needs to be digested in peace and not swept ahead too
soon in a cleaning frenzy. Constant snacking means there is no time
for cleaning. This is part of the reason some nutritional scientists
recommend we leave five hours between meals. There is no
scientific evidence proving that the interval must be precisely five
hours. Those who chew their food thoroughly create less work for
their housekeeper and can listen to their belly when it tells them it’s
time to eat again.
Large Intestine
of the small intestine is a structure known as Bauhin’s
valve. It separates the small from the large intestine, which is good
because the two neighbors have very different ideas about work
ethics. The large intestine is a much more leisurely type. Its motto is
not really “onward, ever onward.” It is not averse to shifting what
remains of our food backward as well as forward if that’s what feels
right at the time. It has no busy little housekeeper. The large intestine
AT THE END
is the tranquil home of our gut flora, which deal with anything that
gets swept into the large intestine undigested.
The large intestine works at a more leisurely pace because it has
to consider several different players. Our brain is picky about when it
wants us to go to the toilet, the bacteria in our gut want ample time to
deal with undigested food, and the rest of our body very much wants
to get back the fluids it lent to the digestive system.
What makes it as far as the large intestine no longer resembles a
piece of cake—nor should it. The unabsorbed remains of the cake
may include a few fruit fibers from the cherry on the top, and the rest
is made up of digestive juices, which are reabsorbed here. When we
are anxious, our brain jockeys the large intestine along, leaving it
without sufficient time to reabsorb all that fluid. The result is diarrhea.
Although the large intestine (like the small intestine) is a smooth
tube, it is always shown in diagrams looking like a lumpy string of
beads. Why is that? In fact, that is just what the large intestine looks
like when the abdomen is opened up. The simple reason for this is
that it is engaged in a slow-motion dance. Just like the small
intestine, it bulges as it processes the food it receives, so as to hold
it where it needs it to be. However, it tends to remain in one position
for a long time without moving—something like those street mimes
who stand in one statuesque pose until someone comes along and
puts a coin in their hat. Every now and then, it relaxes and then
forms bulges in other places. Then it remains in that configuration for
a while. Anatomy books depict it in this way—like a child who blinks
when the class photo is taken to appear in the yearbook looking
dopey forevermore.
Two or three times a day, the large intestine stirs from its
slumbers and gives an enthusiastic shove to the concentrated food
mush to push it forward. Those who provide their large intestine with
sufficient bulk may even have to go to the toilet two or three times a
day. For most people, the content of their large intestine is enough
for one bowel movement a day. But, statistically speaking, three
times a day is still a healthy frequency. Women’s large intestines are
generally slightly more lethargic than men’s. Medical researchers
have not yet discovered why this is so, but the greatest likelihood is
that it has a hormonal cause.
The cake’s journey from fork to toilet takes one day on average.
Faster guts accomplish this journey in eight hours; for slower
digesters, it can take three and a half days. Due to all the mixing
they undergo, some cake particles may linger in the chill-out space
of the large intestine for twelve hours, while others might lounge
around for up to forty-two hours. Leisurely digesters should not worry
as long as the consistency of their bowel movements is fine and they
have no other complaints. On the contrary, one Dutch study showed
that those who belong to the once a day or less faction and those
who have occasional constipation are less likely to contract certain
rectal diseases. This is consistent with the motto of the large
intestine, “Slow and steady wins the race.”
Reflux
THE STOMACH CAN sometimes stumble. Its smooth muscle tissue can
trip up just like the striated muscles of the legs. When that stumble
causes a substance like gastric acid to reach places that are not
designed to deal with it, it hurts. Reflux is the regurgitation of gastric
acid and digestive enzymes into the pharyngeal area; in the case of
heartburn, those juices travel no farther than the end of the
esophagus, causing a burning sensation in the chest.
Reflux has the same cause as stumbling: it’s all down to the
nerves. They control our muscles. If the nerves in our eyes fail to
detect a doorstep in time, our legs receive incorrect information and
carry on walking as if there were no obstacle in the way—and we
stumble. When the nerves of our digestive system receive incorrect
information, they fail to keep our gastric juices where they belong
and allow them to start moving in the wrong direction.
The junction between the esophagus and the stomach is an area
that is particularly susceptible to such stumbles. Despite safety
measures that include a narrow esophagus, a steadied position in
the diaphragm, and the curve at the entrance to the stomach, things
sometimes still go wrong. Around a quarter of people in Europe
regularly experience such problems. This is not just another modern
fad: nomadic people, whose way of life has not changed for
hundreds of years, have similar rates of heartburn and reflux to
Europeans, although rates are thought to be on the rise in the United
States.
The crux of the matter is that two different nervous systems have
to work together in the esophagus and stomach area—the nervous
system of the brain and that of the gut. For example, the sphincter
muscle between the esophagus and the stomach is under the control
of nerves from the brain. The brain also influences gastric acid
production. The nerves of the digestive tract ensure that the
esophagus moves things downward in a harmonious stadium-style
wave, keeping it clean with the thousand-or-so times we swallow
saliva over the course of a day.
Practical tips to help with heartburn and reflux are based on
trying to get those two nervous systems back on the right path.
Chewing gum or sipping tea can help the digestive tract because
small, repeated swallows help nudge the nerves in the right direction
—down toward the stomach, not back up. Relaxation techniques can
help persuade the brain not to send out such hectic instructions via
the nerves. In a best-case scenario, that should result in constant
closure of the sphincter, leading to less acid production.
Cigarette smoke stimulates areas of the brain that are also
activated by eating. This may lead to a sense of satisfaction, but it
also tricks the brain into producing more gastric acid for no practical
reason, as well as causing the sphincter between the esophagus
and the stomach to relax. This is why giving up smoking often helps
reduce reflux and heartburn complaints.
Pregnancy hormones can cause similar disarray. Their intended
function is to keep the womb relaxed and cozy for the unborn baby,
but they also have a similar effect on the sphincter of the esophagus.
The result is a leaky connection to the stomach, which, combined
with the pressure of the bulging belly from below, causes acid to rise.
Contraceptives containing female hormones can cause reflux as a
side effect.
Cigarette smoke or pregnancy hormones—our nerves are not like
fully insulated electric cables. They are embedded organically in our
tissues and react to the substances around them. That’s why many
doctors recommend avoiding foodstuffs that can reduce the strength
of the sealing sphincter: chocolate, hot spices, alcohol, sugary
sweets, coffee, and so on.
All these substances influence our nerves, but they do not
necessarily cause an acid stomach stumble in everybody. The
results of American studies indicate each individual should use trial
and error to find out which foods affect their nerves, rather than
unnecessarily cutting out everything that might be the culprit.
There is an interesting connection discovered by means of a drug
that was never approved because of its side effects. This substance
blocks nerves at a location where glutamate normally binds with
them. Most people are familiar with glutamate as a flavor enhancer,
but it is also released by our nerves. In the nerves of the tongue,
glutamate causes an intensification of taste signals. This can create
confusion in the stomach, since the nerves do not know whether the
glutamate originates from their colleagues elsewhere in the body or
from the local Chinese takeaway. The trial-and-error test here would
involve avoiding food rich in glutamate for a while. To do this, you will
have to take your reading glasses to the supermarket to check those
lists of ingredients in tiny print on food labels. Often, glutamate hides
behind more complicated formulations such as monosodium
glutamate or something similar. If avoiding it results in an
improvement—fine. If not, at least you will have eaten more healthily
for a while.
Those whose stomach stumbles less than once a week can turn
to simple remedies for relief, such as antacids from the pharmacy or
household cures like raw potato juice. Neutralizing stomach acid
should not be used as a long-term strategy, however. Stomach acid
is useful for combating the harmful effects of allergens and bacteria
from our food, and is instrumental in digesting proteins. What is
more, some antacid medications contain aluminum, which is a very
alien substance for our body to deal with. So, overuse of antacids
should be avoided. Always read and follow the instructions on the
leaflet.
Reliance on antacids for four weeks or more should be seen as a
warning sign. Anyone who ignores such warnings will soon feel the
wrath of a disgruntled stomach that wants its acid back—to make up
for the effects of the medication for one thing, but also to return to its
natural acidic state. Antacids are never a long-term solution for reflux
and certainly not for other acidic phenomena, such as gastritis,
which is the medical name for an inflammation of the lining of the
stomach.
When symptoms continue despite the use of antacids, doctors
must get creative to find out why. If blood tests and a thorough
physical examination yield no abnormal results, a doctor may
prescribe a drug called a proton pump inhibitor, or PPI. PPIS inhibit
the production of acid and its secretion into the stomach. Short-term
use of a PI may leave the stomach lacking a little acid, but for those
who suffer from heartburn or reflux, they provide a short respite for
the stomach and the esophagus so that they can recover from the
effects of such acid attacks.
If attacks strike mainly at night, it is a good idea to try propping
the upper body up to an angle of 30 degrees. This can involve
complex pillow constructions and the use of a protractor at bedtime,
but specially manufactured pillows are also available from specialist
suppliers. Incidentally, a 30-degree upper body inclination is also
good for the cardiovascular system. My old physiology professor
never tired of telling us this, and, given that his specialty is
cardiovascular research, I am more than inclined to believe him. But
it also means I now can’t help imagining him propped up in bed
every time someone mentions his name.
Patients should lose sleep over such serious warning signs as
difficulty swallowing, weight loss, swelling, or any sign of blood.
When such symptoms appear, it is high time for an exploratory
expedition into the stomach with a camera—no matter how
unpleasant an experience that can be. The real danger with reflux
comes not, in fact, from burning acid, but from bile reaching the
esophagus from the small intestine via the stomach. Bile does not
cause a burning sensation, but it has much more insidious effects
than acid. Luckily, for most people who suffer from reflux, there is
very little bile involved.
The presence of bile can seriously confuse the cells of the
esophagus. Suddenly, they are no longer sure where they are,
thinking, “Am I really an esophagus cell? I keep sensing bile!
Perhaps I’ve really been a small intestine cell all these years without
realizing it . . . Silly me!” Anxious to do the right thing, they change
from esophagus cells into gastrointestinal cells. That can cause
problems. Mutating cells can make mistakes in their own programing
and no longer grow in a controlled way like other cells. However, this
has serious repercussions for only a small percentage of people who
suffer from stomach stumbles.
In the vast majority of cases, reflux and heartburn are stumbles
that are unpleasant but not dangerous. When we stumble while
walking, we usually briefly adjust our clothing, neutralize the shock
with a shake of the head, and walk on at a measured pace. The
same reaction is appropriate in the case of an acid stumble of the
stomach—a couple of mouthfuls of water for adjustment, neutralize
the acid if necessary, and then continue walking, perhaps at a less
hectic pace.
Vomiting
IF YOU TOOK a hundred people on the verge of vomiting, you would
have a very mixed group. Person number 14 is on a rollercoaster,
hands high in the air, person 32 is cursing the egg salad she ate,
number 77 is holding a pregnancy test in disbelief, and number 100
has just read the words “may cause nausea and vomiting” in the
leaflet that came with his new medication.
Vomiting is not a stomach stumble: it happens according to a
precise plan. It is a tour de force performance. Millions of tiny
receptors test our stomach contents, examine our blood, and
process impressions from the brain. Every piece of information is
gathered in the huge fibrous network of our nervous system and sent
to the brain. The brain evaluates this information. Depending on how
many alarm bells are ringing, it makes a decision: to barf or not to
barf. The brain transmits its decision to selected muscle groups, and
they get down to work.
If you were to X-ray the same hundred people while they were
vomiting, the picture would be the same a hundred times over. The
brain responds to the alarm, activates the area responsible for
vomiting, and switches the body to emergency mode. We turn pale
as the blood drains from our cheeks and is sent to the abdomen. Our
blood pressure drops and our heart rate falls. Finally, we feel that
unmistakable sign: saliva, and lots of it. The mouth begins producing
saliva in great quantities as soon as it receives information from the
brain about the emergency that’s underway. This saliva is meant to
protect our teeth from the corrosive effects of the gastric acid they
are about to come into contact with.
To begin with, the stomach and gut move in small, nervous
waves—shoving their contents in completely opposite directions as
they begin to panic slightly. We cannot feel this to-and-fro as it takes
place in the realm of smooth muscle; however, this is about the time
that most people realize intuitively that they should seek out a
suitable receptacle.
An empty stomach is no defense against vomiting, since the
small intestine is just as able to expel its contents. For this to
happen, the stomach opens the gate to allow the contents of the
small intestine back in. Every member of the team works together to
bring this major project to completion. When the small intestine
suddenly sweeps its contents into the stomach, sensitive nerves
there are stimulated. These nerves respond by sending signals to
the vomit control center in the brain. Now there’s no doubt about it:
everything is ready for the big heave.
Our lungs take a particularly large breath before our airways are
closed. The stomach and the opening to the esophagus suddenly
relax and—bam!—the diaphragm and abdominal muscles abruptly
press upward, squeezing us like a tube of toothpaste. The entire
contents of the stomach are then propelled from the body like a pilot
in an ejector seat.
Why We Vomit and
What We Can Do to
Prevent It
is especially designed to be able to vomit. Other
animals with this ability include apes, dogs, cats, pigs, fish, and
birds. Those that are not able to vomit include mice, rats, guinea
pigs, rabbits, and horses. Their esophagus is too long and narrow,
and they lack the nerves that are so talented at vomiting.
Animals that cannot vomit have to have different eating habits
from ours. Rats and mice nibble at their food, biting off tiny pieces to
test their suitability. They only continue to eat when they are sure the
trial nibble has not done them any harm. If it turns out to be toxic, the
most they suffer will be a bout of stomachache. They also learn not
to eat it again. Furthermore, rodents are much better than us at
breaking down toxins because their liver has more of the necessary
enzymes. Horses, however, are not even able to nibble. If something
bad ends up in their small intestine, the results can often be life
threatening. So, really, we have reason to be proud of our body’s
abilities whenever we find ourselves crouched over the toilet bowl
“throwing our guts up.”
The short rests between retches could be utilized for a little
reflection. Person number 32’s notorious egg salad seems to have
held its form surprisingly well when it returns from its short sojourn in
the realm of the stomach. A few pieces of egg, the odd pea or piece
of pasta are still recognizable. It might cross 32’s mind that she can’t
have chewed it very well. Moments later, another retch produces
rather more deconstructed arrangement. Vomit that contains
recognizable bits of food is almost certain to have originated from the
stomach and not from the small intestine. The smaller the particles,
the more bitter the taste, and the more yellow the color, the more
likely it is to be a salutation from the small intestine. Clearly
identifiable food may not have been chewed properly, but at least it
has been ejected from the stomach quickly, before making it as far
as the small intestine.
THE HUMAN ANIMAL
The way we vomit also tells us quite a bit. Sudden vomiting that
comes in a violent surge almost without warning is likely to be
caused by a gastrointestinal virus. This is due to the fact that the
sensors count how many pathogens they encounter and when they
decide the numbers have got out of hand, they slam on the
emergency brakes. Below this threshold, the body’s immune system
could likely have dealt with the situation, but now the job is handed
over to the gastrointestinal muscles.
Food poisoning and alcohol poisoning also cause vomiting in
surges. However, this time we usually get a fair warning beforehand,
in the form of nausea. The feeling of nausea is the body’s way of
telling us that the food we have eaten is not good for us. Person 32
is likely to be much more wary of that bowl of egg salad on the buffet
in future.
Person 14 on the rollercoaster feels just as nauseous as number
32 of egg salad fame. Rollercoaster puking is basically the same as
travel sickness. In this case, no toxins are involved, yet sick still ends
up on people’s shoes, in the glove compartment, or splattered on the
back window by the force of momentum. The brain is the bodyguard
of the body—guarding it meticulously and cautiously, especially
when the body belongs to a small child. Currently, the best
explanation of motion sickness is this: when the information sent to
the brain from the eyes is at odds with that sent by the ears, the
brain cannot understand what is going on and slams on every
emergency brake at its disposal.
When a passenger reads a book in a moving car or train, their
eyes register “hardly any motion,” while the balance sensors in the
ears say “lots of motion.” It’s the same, but opposite, effect as when
you watch the trees whizz by when driving through a forest. If you
move your head a little as well, it looks as if the trees are rushing by
faster than you are actually moving—and that, too, confuses the
brain. On an evolutionary scale, our brains are familiar with such
mismatches between eyes and balance sensors as signs of
poisoning. Anyone who has ever drunk too much or taken drugs will
have felt the room spinning, even when they are not moving at all.
Vomiting can also be caused by intense feelings such as
emotional strain, stress, or anxiety. Under normal circumstances, we
synthesize the stress-response hormone CRF (corticotropinreleasing factor) in the morning, creating a supply to help face the
challenges of the day. CRF helps us tap into energy reserves,
prevents the immune system from overreacting, and helps our skin
tan as a protective response to stress from sunlight. The brain can
also inject an extra portion of CRF into the bloodstream if we find
ourselves in a particularly upsetting situation.
However, CRF is synthesized not only by brain cells, but also by
gastrointestinal cells. Here, too, the signal is—stress and threat!
When gastrointestinal cells register large amounts of CRF,
irrespective of where they originate (in the brain or in the gut), the
information that one of the two is overwhelmed by the outside world
is enough for the body to react with diarrhea, nausea, or vomiting.
When the brain is stressed, vomiting expels partly digested food
in order to save the energy required to complete the digestive
process. The brain can then use that energy to solve the problems at
hand. When the gut is stressed, partly digested food is ejected either
because it is toxic or because the gut is currently not in a position to
digest it properly. In both cases, it can make good sense to press the
eject button. There is simply no time for gentle, comfortable
digestion. When people throw up from nerves, it is simply their
digestive tract trying to do its best to help.
Incidentally, petrels use vomiting as a defense strategy. Vomiting
is a sign from the plucky little birds to steer well clear of their nests.
Researchers use that to their advantage. They approach a petrel’s
nest holding out a barf bag, and the seabird pukes right into it. Back
at the lab, they can test the petrel vomit for anything from the
presence of heavy metals to the variety of fish it contains. This gives
them a measure of how healthy the environment is.
The following includes some simple strategies for reducing
unnecessary attacks of vomiting.
1. For travel sickness, keep your eyes fixed on the horizon far
ahead. This helps the eyes and balance sensors coordinate their
information better.
2. Listen to music on headphones, lie on your side, or try relaxation
techniques—some people find this helpful. One possible
explanation for this is that all these activities are generally
calming. The more secure we feel, the less we encourage the
brain’s state of alarm.
3. There are now quite a few studies proving that ginger has a
beneficial effect. Substances contained in root ginger block the
vomit center of the brain and the feeling of nausea along with it.
Many ginger candies, however, contain only ginger flavoring, so
make sure anything you take contains the genuine stuff.
4. Drugs you can buy from the pharmacy to prevent vomiting work in
various ways. They can block the receptors in the vomit center
(the same effect as ginger), numb the nerves of the stomach and
gut, or suppress certain alarm signals. The drugs in the last group
are almost identical to drugs used to treat allergies. Both
suppress the alarm-signal transmitter histamine. However, the
drugs used to prevent vomiting have a much stronger effect on
the brain. Modern allergy drugs have been developed and
improved to such a degree that they barely dock in the brain at all.
This interaction with the brain is what makes the suppression of
histamines cause drowsiness.
5. P6! This is an acupuncture point that is now recognized by
Western medicine as effective against nausea and vomiting. Its
benefits have been proven in more than forty studies, including
placebo-controlled trials. Doctors do not know how or why P6
works. The point is located two to three finger-breadths below the
wrist, right between the two prominent tendons of the lower arm. If
you don’t happen to have an acupuncture needle handy, you can
try gently stroking the skin at that point until symptoms improve.
This technique has not been proven in scientific studies, but it
may be worth trying a little self-experimentation. In traditional
Chinese medicine, stimulating this point is believed to activate the
energy pathway, or meridian, running up the arm and through the
heart, which relaxes the diaphragm and then runs on through the
stomach and into the pelvis.
will work for all causes of nausea. Remedies like
ginger, pharmacy-bought medicines, or P6 can help, but for vomiting
caused by emotional factors, the best thing is often to build a safe
nest for your own inner petrel. Relaxation techniques or
hypnotherapy (from a reputable practitioner!) can help train the
NOT EVERY STRATEGY
nerves to be more thick-skinned. The more often and the longer you
practice, the better you will get. Silly stress at the office or examrelated anxiety become less threatening when we refuse to let these
stressors affect us so personally.
Vomiting is never a punishment from the stomach! Rather, it is a
sign that our brain and our gut are willing to sacrifice themselves to
the ultimate extreme for us. They protect us from unseen toxins in
our food, are overcareful when faced with travel-related eye–ear
hallucinations, and save energy to deal with imminent problems.
Nausea is meant to give us an orientation for the future, letting us
know what is good for us and what is bad.
If you are unsure about the cause of your nausea, it is a good
idea to simply trust your gut feeling. The same principle applies
when you have eaten something bad but don’t feel the need to
vomit. You should not force the situation with a finger down your
throat, by drinking salt water, or by having your stomach pumped.
Taking acidic or foaming chemicals can cause more problems than it
solves. Foam can easily migrate from the stomach to the lungs, and
acidic drugs may simply burn the esophagus for a second time. For
these reasons, induced vomiting is no longer a technique normally
recommended for use in modern emergency medicine.
True nausea is a program that has evolved over many millennia
—it has the ability to wrest the reins of control from our conscious
mind. The conscious mind often reacts to this drastic takeover with
shock and indignation. It was blithely planning to order another round
of tequila shots—and now this? But, since it is often the conscious
mind that got the body into this vomitous situation in the first place, it
eventually has to back down. If vomiting is caused by an
unnecessary, overcautious reaction, the conscience mind can always
return to the negotiating table and play its anti-vomiting aces.
CONSTIPATION CONSTIPATION IS LIKE. You wait for something that just
won’t. And, still you have to use a lot of force. Sometimes, in
return for all that effort, you get no more than • • • . Or it works, but
not very
OFTEN.
Between 10 and 20 percent of people in the United States are
constipated. If you want to join this club, you must fulfil at least one
of the following conditions: bowel movement less than three times a
week; particularly hard stool a quarter of the time, often in pellet form
( • • • ), which is difficult or impossible to pass without help
(medication or tricks); no satisfying feeling of emptiness on leaving
the toilet.
Constipation results from a disconnect between the nerves and
the muscles of the gut when they are no longer working toward quite
the same goal. In most cases, digestion and transportation of food
through the system are still working at normal speed. It is not until
the very end of the large intestine that disagreement arises as to
whether the contents need to be expelled right away or not.
The best parameter for assessing constipation is not how often
you need to go to the toilet, but how difficult it is. Time spent sitting
on the toilet is supposed to be a time of splendid isolation and
relaxation, but for those whose experience is not so laid back, it can
be a troubling time. There are various levels of constipation.
Temporary constipation can be due to traveling, illness, or periods of
stress. More obstinate constipation can indicate more long-term
problems.
Almost half of us have experienced constipation when traveling.
Particularly in the first few days of a trip, it is often difficult to go
properly. This can be due to a variety of reasons, but in most cases it
boils down to the simple fact that the gut is a creature of habit. The
nerves of the gut remember what kind of food we prefer and at what
time we prefer to eat it. They know how much we move around and
how much water we drink. They know whether it is day or night and
what time we usually go to the toilet. If everything goes according to
plan, they complete their tasks without complaint and activate our
gut muscles to help us digest.
When we travel, we have a lot on our mind. Did we pick up our
keys and turn off the iron? We might remember to take a book or
some music to keep our brains happy, but there is one thing we
always forget—that creature of habit, the gut, is also traveling with us
and is suddenly torn from its familiar routine.
We spend the whole day eating prepackaged sandwiches,
strange airplane meals, or unfamiliar spices. At the time we would
normally be enjoying our lunch break, we’re stuck in traffic or waiting
at the check-in counter. We drink less than normal, for fear of having
to go to the toilet too often, and dehydrate even more during the
flight. And, as if that weren’t enough, we might also have to face a
big fat bout of jetlag.
All this does not go unnoticed by the nerves of the gut. They can
get confused and put the brakes on until they receive a signal that
everything is normal and they can start work again. Even when the
gut has done its work despite the confusion, and signals to us that
we should seek out the toilet, we add to its woes by suppressing the
urge because it happens not to be a convenient time. Also, if we’re
honest, travel constipation can often be caused by the “not my toilet”
syndrome. Sufferers of this syndrome simply dislike doing their
business in unfamiliar toilets. Their biggest challenge is posed by
public conveniences. Many people use them only when it’s
absolutely necessary, construct elaborate seat sculptures out of toilet
paper, or crouch what feels like miles away from the toilet bowl. But
even all that doesn’t help those with a serious case of “not my toilet”
syndrome. They simply cannot relax enough to finish the work their
creature of habit has begun. When that happens, a holiday or
business trip can become a rather unpleasant experience.
THERE ARE A FEW little tricks that can be useful for people with
brief or mild instances of constipation. These tricks can lower
inhibitions and help get things moving in the bowel department.
1. There is a certain foodstuff we can eat to nudge the gut wall into
action: fiber. Dietary fiber is not digested in the small intestine and
can knock on the wall of the large intestine in a friendly way to say
there is someone here who wants to be shown the way out. The
best results are produced by psyllium seed husks and the rather
more pleasant-tasting plum. Both contain not only fiber, but also
agents that draw extra fluids into the gut—making the whole
business smoother. It can take two to three days before their
effect is felt. So, you can start eating them either a day before
your trip or on the first day—whatever feels safer. Those with no
plum compartment in their suitcase can buy dietary fiber in tablet
or powdered form from their pharmacy or drug store. One ounce
(30 grams) is an appropriate daily dose of dietary fiber.
There are two kinds of fiber: water-soluble and insoluble. The
latter is better at stimulating movement through the digestive
system, but it can often cause stomachaches. Water-soluble fiber
does not provide quite such a powerful push, but it does make the
contents of the gut softer and easier to deal with. Nature’s design
is rather clever: the skins of many fruits contain large amounts of
insoluble fiber, while the flesh of the fruit contains more soluble
fiber.
Consuming dietary fiber is little help if you do not also
consume sufficient fluids. Without the presence of water, fiber
binds together in solid lumps. Water makes them swell up into
balls. This gives the bored gut something to do while your brain
enjoys the in-flight entertainment.
2. Drinking more fluids can only help those who don’t already drink
enough. For those who do, drinking even more will not bring
about any improvement. But it is a different story if the body gets
too little fluid. The gut reacts by extracting more water from the
food passing through it. That makes the feces harder. Small
children running high temperatures often lose so much body fluid
through sweating that their digestive system grinds to a halt. Air
travel can cause the body to lose similar quantities of water, even
without sweating. The air in the plane is so dry that it extracts fluid
from our body without our even noticing. The first sign we have of
it is an unusually dry nose. During air travel it is a good idea to try
to drink more than normal to keep the water in your body at a
normal level.
3. Don’t put yourself under pressure. If you need to go to the toilet,
just go—especially if you are a creature of habit like your gut and
usually go at an appointed time. If you normally go to the toilet in
the morning but suppress the urge because you’re traveling, it is
as if you have broken an unspoken agreement with your gut. You
gut likes to work according to plan. Pushing digested food back
into a holding pattern even just a couple of times trains the nerves
and muscles to operate in reverse gear. That can make it
increasingly difficult to change gears back again. This is
compounded by the fact that the longer the feces stay in the gut,
the more time the body has to extract fluid from them, making the
business ever harder. A couple of days of suppressing the urge
can lead to constipation. So, if you still have another week of your
camping holiday to go, you’d better get over your fear of the
communal toilets before it’s too late!
4. Probiotics and prebiotics—living, beneficial bacteria and their
favorite food—can breathe new life into a tired gut. It is a good
idea to consult your pharmacist about this or turn to the sections
on probiotics and prebiotics later in this book.
5. Take more walks? That is not always a successful strategy. A
sudden decrease in exercise can cause the gut to slow down, it’s
true. But for those who already exercise enough, more movement
will not help them attain digestive nirvana. Tests have shown that
it takes extremely strenuous exercise to achieve a measurable
effect on the movement of the gut. So, unless you are planning to
engage in some kind of power sport, forcing yourself to take an
extra walk will have little effect—on your ability to go to the toilet
successfully, at any rate.
THOSE WITH A taste for the unusual might want to try the rocking
squat technique. Sitting on the toilet, bend your upper body forward
as far as possible toward your thighs, then straighten up to the sitting
position again. Repeat this a few times and it should begin to work.
No one watches you while you are on the toilet and you have a
moment of free time, so what could be a better opportunity for an
unusual experiment?
HERE ARE SOME strategies for times when household remedies
and rocking on the toilet fail.
In more stubborn cases of constipation, the nerves of the gut are
not just confused or sulking, they are in need of a bit more support
from their owner. If you have tried all the little tips and still don’t leave
the toilet singing a merry tune, it may be time to rummage in another
box of tricks. But you should only do this if you already know the
reason for your problem. If you don’t know the precise cause of your
constipation, you cannot choose the right remedy.
If constipation comes on very suddenly or lasts for an unusually
long time, you must consult your doctor. The problems may stem
from undiagnosed diabetes or thyroid problems, or you may just be a
natural-born slow transporter.
Laxatives
taking laxatives is easily stated: to produce the perfect
little pile. Laxatives can coax even the shyest gut out of its shell.
Laxatives come in various types, which work in different ways. For all
hopelessly constipated travelers, slow transporters, campsite toilet
objectors, or hemorrhoid-hindrance conquerors, here’s a look at that
box of tricks.
THE AIM OF
The Perfect Little Pile by Means of Osmosis . . . IS WELL formed
and not too hard. Osmosis is water’s sense of equality. When one
region of water contains more salt, sugar, or similar substances than
another, the less rich water will flow toward the richer water until both
contain the same amount of solute and they can live on in peaceful
equilibrium. The same principle helps to revive wilting lettuce—
simply soak the sad salad in water and half an hour later your greens
will be crispy again. Water flows into the lettuce because its cells
contain more salts, sugars, and so on than the pure water in the
bowl.
Osmotic laxatives use the same principle of equality. They
contain certain salts, sugars, or tiny molecular chains that can travel
into the large intestine. Along the way, they gather all the water they
can to make the act of going to the toilet as comfortable as possible.
But overdoing it with such laxatives causes them to extract too much
water. Diarrhea is a sure sign that you have taken too many.
With osmotic laxatives, you can choose whether to take sugars,
salts, or short molecular chains to help retain water in the gut. The
salts, such as sodium sulfate (also known as Glauber’s salt) are
rather rough on us. They take effect very suddenly, and if they are
taken too often, they disrupt the body’s electrolyte balance.
The most widely known laxative sugar is lactulose. It has a useful
double effect, both retaining water in the large intestine and feeding
the flora of the gut. Those little creatures can help, for example, by
producing some substances that act as stool softeners and others
that stimulate movement in the gut wall. But this can also cause
unpleasant side effects. Overfed or misplaced bacteria can produce
gases, causing cramps and flatulence.
Lactulose is formed from the milk sugar, lactose, when milk is
heated to high temperatures. Pasteurization involves heating milk
briefly, so pasteurized milk contains more lactulose than raw milk.
UHT (ultra-high-temperature-processed) milk contains more
lactulose than pasteurized milk, and so on. Non-milk laxative sugars
are also available, including sorbitol. Sorbitol occurs naturally in
some kinds of fruit—plums, pears, and apples, for example. That is
one reason for the reputation plums have as a natural laxative and
for warnings that too much fresh apple juice can cause diarrhea.
Since human beings can barely absorb sorbitol (or lactulose) into
their bloodstream, it is often used as a sweetening agent. It then
appears on food labels as E420, and this explains why sugar-free
cough candies, for example, always include the warning, “Excessive
consumption may have a laxative effect.” Some studies have shown
that sorbitol has a similar effect to lactulose, but causes fewer side
effects overall (no unpleasant wind).
Of all laxatives, the short molecular chains are most easily
tolerated by the body. They have the kind of complicated names that
molecular chains love—polyethylene glycol, for example, known as
PEG for short. They don’t disrupt the body’s electrolyte balance like
salts do, and they do not produce wind like sugars do. The length of
the chain is often included in the name: PG-3350, for example, is a
chain made up of enough atoms to give it the molecular weight 3350.
It is much better than PEG-150, because that compound is made of
such short chains that they can be inadvertently absorbed by the gut
wall. That might not necessarily be dangerous, but it can certainly
confuse the nerves of the gut, since polyethylene glycol is definitely
not part of our natural diet.
For this reason, short chains like PEG-150 are not contained in
laxatives, but they are used in products such as skin cream, where
they perform a very similar service—they make the skin more
supple. It is unlikely that they are harmful, but the matter is still not
finally settled. Laxatives based on PEGs contain only indigestible
chains, and for that reason they can be taken over longer periods
without causing problems. The latest studies show there is no risk of
addiction or long-term damage. Some studies indicate that these
substances can even improve the gut’s protective barrier.
Osmotic laxatives work not only by making the feces moister, but
also by sheer mass. The more moisture, well-fed gut bacteria, or
molecular chains are contained in the gut, the more motivated it will
be to move. This is the basic principle of the peristaltic reflex.
The Perfect Little Pile by Means of Slippery Stool . . . SOUNDS
LIKE A children’s party game. Slippery stool—lots of fun but maybe
quite messy. But in fact this is the technique known medically as
fecal lubrication. Robert Chesebrough, the man who invented
Vaseline®, swore by a spoonful of the petroleum jelly every day.
Swallowing petroleum jelly probably has the same effect as
swallowing other fat-based fecal lubricants—an overdose of
indigestible fat coats the goods in transit, making for an easier exit.
Chesebrough lived to the ripe old age of ninety-six, which is quite
surprising since eating a fat-based lubricant every day will cause the
body to lose too many fat-soluble vitamins. They get covered in the
fatty lubricant and go the same way as the feces. This can cause
vitamin deficiencies that lead to illness, especially if fecal lubricants
are taken too often or in excessive amounts. Petroleum jelly is not
one of the official fecal lubricants (and really shouldn’t be eaten), but
the time-honored candidates such as liquid paraffin are hardly less
suitable for regular use. They can be useful as short-term treatments
—for example, in the presence of hemorrhoids or small but painful
injuries to the anus. In such cases, it can be good to make the feces
softer to avoid pain or further injury during defecation. However, gelforming fibers available from the pharmacy do just as good a job and
are less dangerous and better for the body.
The Perfect Little Pile by Means of Hydragogues . . . IS
ACHIEVED by giving the gut a big kick up the butt. These laxatives
are ideal for those with very shy, lethargic gut nerves. There are
various tests to find out whether that applies to you. One test
involves swallowing little medical pellets that doctors then X-ray as
they pass through the gut. If, after a certain time, the pellets are still
spread throughout the tract, having failed to gather by the back door
as they should, hydragogues are the appropriate treatment.
Hydragogues latch onto a couple of the receptors that the gut
waves around inquisitively. They then send signals to the gut to stop
extracting fluid from the food passing through and to fetch more
water from other parts: muscles—shake a leg! To put it bluntly,
cleverly constructed hydragogues simply boss nerve cells and water
transporters around. When osmotic laxatives fail to provide enough
stimulus or softness, a shy gut needs a few clear commands. If
hydragogues are taken before bedtime and left to do their thing
overnight, the gut will react the next morning. If time is an issue, the
express mail service of a suppository can usually deliver the
message within half an hour.
The commando squad need not rely on chemical weapons—
some plants work in much the same way. These include aloe vera
and senna, for example. But they do have one rather interesting side
effect. Anyone who has ever wished to dye the inside of their gut
black is welcome to have a go. This discoloration is not dangerous,
and it fades with time.
Hydragogues encourage the gut to keep things moving in the right direction.
However, some scientists have reported effects of an excess of
hydragogues or aloe vera that would be rather less fun—if they turn
out really to be caused by those substances—as they include
damage to the nerves. The reason is that nerves that are bossed
around too much eventually become overwrought. When that
happens, they withdraw into themselves, like snails when you tap
their feelers. For this reason, patients with long-term problems
should not take hydragogues more than every two or three days.
The Perfect Little Pile by Means of Prokinetics
. . . IS THE very latest thing—for two reasons. These drugs can only
support the gut in doing what it naturally does anyway, and they
cannot issue any unwanted orders. They work along the same lines
as a loudspeaker. The exciting thing for many scientists is that they
can help in an extremely targeted way. Some prokinetic agents affect
only one single receptor, while others are not absorbed into the
bloodstream at all. However, scientists are still researching the way
many of these substances work, and new ones are just now
appearing on the market. So, anyone who does not absolutely need
to try something new should stay on the safe side and rely on bettertested drugs for now.
The Three-Day Rule
laxatives without explaining the three-day
rule, although it is easy to remember and is a useful aid. The large
intestine has three sections: the ascending, transverse, and
descending colon. When we go to the toilet, we usually empty the
last section. By the next day, it has filled up again and the game
starts all over again. Taking a strong laxative may cause the entire
large intestine—all three sections—to be emptied. It can then easily
take three days before the large intestine is full again.
MANY DOCTORS PRESCRIBE
1. Normal situation: one-third of the large intestine is emptied and it is full again by the next
day.
2. After taking a laxative: the entire large intestine is emptied and it may take three days to
fill up again.
Those unfamiliar with the three-day rule will likely start to get
nervous during that time. Still no bowel movement? And before they
know it, they’ve taken the next laxative tablet or powder. This is a
vicious and unnecessary circle. After taking a laxative, the gut
deserves a couple of days’ respite. Monitoring for normal bowel
movements should begin on the third day. Slow transporters may
need to give a helping hand to their gut after two days.
The Brain and the Gut
THIS IS A sea squirt.
It may be enlightening to learn the sea squirt’s view on the
necessity of having a brain. The sea squirt, like humans, is a
member of the chordate phylum. It has a bit of a brain and a kind of
spinal cord. The brain blithely sends messages to the rest of the
body via the spinal cord and receives interesting information in
return. In humans, for example, it might receive an image of a traffic
sign from the eyes; a sea squirt’s eyes might tell it when a fish swims
by. A human’s brain might receive information from the sensors in
the skin about whether it’s cold outside; a sea squirt’s skin sensors
can tell its brain about the temperature of the water deeper in the
sea. A human might get information about whether certain foods are
good to eat . . . and so might a sea squirt.
Equipped with all this information, a young sea squirt navigates
the great oceans until it finds a rock that is secure, located in water
that is just the right temperature, and surrounded by food. Having
found a home, the sea squirt settles down. Sea squirts are sessile
animals: once they take up residence, they never move again, no
matter what happens. The first thing a sea squirt does after setting
up home is to eat its own brain. And why not? It’s possible to live and
be a sea squirt without one.
Daniel Wolpert is not only an engineer and medical doctor who
has won many academic honors, he is also a scientist who believes
the sea squirt’s attitude to having a brain is very significant. His
theory is that the only reason for having a brain is to enable
movement. On first hearing, that might sound like an annoyingly
mundane statement. But perhaps we just consider the wrong things
mundane.
Movement is the most extraordinary thing ever developed by
living creatures. There is no other reason for having muscles, no
other reason for having nerves in those muscles, and probably no
other reason for having a brain. Everything that has ever been done
in the history of humankind was only possible because we are able
to move. Movement is not just walking or throwing a ball. It is also
pulling faces, uttering words, and putting plans into action. Our brain
coordinates its senses and creates experience in order to produce
movement: movement of the mouth or the hands, movement over
many miles or over just a few inches. Sometimes, we can also
influence the world around us by suppressing movement. But if
you’re a tree and can’t choose whether you move or not, you don’t
need a brain.
The common or garden sea squirt no longer needs a brain after it
has settled in one place. Its time of movement is over, and so its
brain is surplus to requirements. Thinking without moving is less
useful than having a mouth opening to eat plankton with. The latter
influences the balance of nature at least a tiny bit.
We humans are very proud of our particularly complex brains.
Thinking about constitutional law, philosophy, physics, or religion is
an impressive feat and can prompt extremely sophisticated
movements. It is awe-inspiring that our brains are capable of all this.
But at some point, that awe wears off, and we hold our brains
responsible for everything we experience in life—we think up
experiences of well-being, happiness, or satisfaction inside our own
heads. When we are insecure, anxious, or depressed, we worry that
the computer in our heads might be broken. Philosophizing and
physics research are matters of the mind and always will be—but
there is more to our self than that.
And it is from the gut that we learn this lesson—the organ that is
responsible for little brown heaps and unbidden sounds and smells
of all sorts. This is the organ that is currently forcing researchers to
rethink. Scientists are cautiously beginning to question the view that
the brain is the sole and absolute ruler over the body. The gut not
only possesses an unimaginable number of nerves, those nerves are
also unimaginably different from those of the rest of the body. The
gut commands an entire fleet of signaling substances, nerveinsulation materials, and ways of connecting. There is only one other
organ in the body that can compete with the gut for diversity—the
brain. The gut’s network of nerves is called the “gut brain” because it
is just as large and chemically complex as the gray matter in our
heads. Were the gut solely responsible for transporting food and
producing the occasional burp, such a sophisticated nervous system
would be an odd waste of energy. Nobody would create such a
neural network just to enable us to break wind. There must be more
to it than that.
We humans have known since time immemorial something that
science is only now discovering: our gut feeling is responsible in no
small measure for how we feel. We are “scared shitless” or we can
be “shitting ourselves” with fear. If we don’t manage to complete a
job, we can’t get our “ass in gear.” We “swallow” our disappointment
and need time to “digest” a defeat. A nasty comment leaves a “bad
taste in our mouth.” When we fall in love, we get “butterflies in our
stomach.” Our self is created in our head and our gut—no longer just
in language, but increasingly also in the lab.
How the Gut Influences the Brain
feelings, they start out by looking for
something to measure. They draw up scales for suicidal tendencies,
test hormone levels to measure love, or set up trials for tablets to
treat anxiety. To outsiders, this often appears less than romantic. In
Frankfurt, there was even a study that involved scanning the brains
of volunteers while a research assistant tickled their genitals with a
toothbrush. Such experiments tell scientists which areas of the brain
receive signals from which parts of the body. This helps them draw a
map of the brain.
So they now know, for example, that signals from the genitals are
sent to the upper central part of the brain, just below the crown. Fear
is found in the middle of the brain—right between the ears, so to
speak. Word formation is located just above the temple. Morality is
WHEN SCIENTISTS STUDY
located behind the forehead, and so on. In order to improve our
understanding of the relationship between the gut and the brain, we
must trace their communication pathways. How do signals get from
belly to brain, and what effect do they have when they get there?
Signals from the gut can reach different parts of the brain, but
they can’t reach everywhere. For example, they never end up in the
visual cortex at the back of the brain. If they did, we would see visual
effects or images of what is going on in our gut. Regions they can
end up in, however, include the insula, the limbic system, the
prefrontal cortex, the amygdala, the hippocampus, and the anterior
cingulate cortex. Any neuroscientists reading this will be up in arms
when I roughly define the responsibilities of these brain regions as,
respectively, self-awareness, emotion, morality, fear, memory, and
motivation. This does not mean that our guts control our moral
thinking, but it allows for the possibility that the gut might have a
certain influence on it. Scientists need to conduct more laboratory
experiments to look more closely at that possibility.
The forced swimming test, carried out on mice, is one of the most
revealing experiments performed in the name of research into
motivation and depression. A mouse is placed in a small container of
water that is too deep for it to reach the bottom with its feet, forcing it
to swim around trying in vain to get to dry land. The question is, how
long will it keep swimming in pursuit of its aim? This boils down to
one of the basic questions of our existence: how intensely are we
prepared to strive for something that we believe exists? That might
be something concrete, like dry land beneath our feet or high school
graduation. Or it might be something abstract, like satisfaction or
happiness.
Areas of the brain activated by vision, fear, word formation, moral thought, and genital
stimulation.
Mice with depressive tendencies do not swim for long. They
simply freeze, apathetically awaiting their fate. It seems inhibitory
signals are transmitted more efficiently in their brains than
motivational or driving impulses. Such mice also show a stronger
reaction to stress. New antidepressants can normally be tested on
these mice. If they swim for longer after receiving the medication, it
is an indication that the substance under scrutiny might be effective.
Researchers in the team, led by the Irish scientist John Cryan,
took this one step further. They fed half their mice with Lactobacillus
rhamnosus (JB-1), a strain of bacteria known to be good for the gut.
Back in 2011, the idea of altering the behavior of mice by changing
the contents of their gut was very new. And, indeed, the mice with
the enhanced gut flora not only kept swimming for longer and with
more motivation, but their blood was also found to contain fewer
stress hormones. Furthermore, these mice performed better in
memory and learning tests than their unenhanced peers. When
scientists severed their vagus nerve, however, no difference was
recorded between the two groups of mice.
The vagus nerve is the fastest and most important route from the
gut to the brain. It runs through the diaphragm, between the lungs
and the heart, up along the esophagus, through the neck to the
brain. Experiments on humans have shown that people can be made
to feel comfortable or anxious by stimulating their vagus nerve at
different frequencies. In 2010, the European Union approved a
medical treatment that uses stimulation of the vagus nerve to help
patients suffering from depressive disorders. So, this nerve works
something like a telephone connection to the switchboard at a
company’s headquarters, transferring messages from staff out in the
field.
The brain needs this information to form a picture of how the
body is doing. This is because the brain is more heavily insulated
and protected than any other organ in the body. It nestles in a bony
skull, surrounded by a thick membrane, and every drop of blood is
filtered before it is allowed to flow through the regions of the brain.
The gut, by contrast, is right in the thick of it. It knows all the
molecules in the last meal we ate, inquisitively intercepts hormones
as they swim around in the blood, inquires of immune cells what kind
of day they’re having, and listens attentively to the hum of the
bacteria in the gut. It is able to tell the brain things about us it would
never otherwise have had an inkling of.
The gut has not only a remarkable system of nerves to gather all
this information, but also a huge surface area. That makes it the
body’s largest sensory organ. Eyes, ears, nose, or the skin pale by
comparison. The information they gather is received by the
conscious mind and used to formulate a response to our
environment. They can be seen as life’s parking sensors. The gut, by
contrast, is a huge matrix, sensing our inner life and working on the
subconscious mind.
Cooperation between the gut and the brain begins very early in
life. Together, they are responsible for a large proportion of our
emotional world when we are babies. We love the pleasant feeling of
a full stomach, get terribly upset when we are hungry, or grizzle and
moan with wind. Familiar people feed, change, and burp us. It’s
palpably clear that our infant self consists of the gut and the brain.
As we get older, we increasingly experience the world through our
senses. We no longer scream blue murder when we don’t like the
food at a restaurant. But the connection between gut and brain does
not disappear overnight, it simply becomes more refined. A gut that
does not feel good might now subtly affect our mood, and a healthy,
well-nourished gut can discreetly improve our sense of well-being.
The first study of the effect of intestinal care on healthy human
brains was published in 2013—two years after the study on mice.
The researchers assumed there would be no visible effect in
humans. The results they came up with were surprising not only for
them, but for the entire research community. After four weeks of
taking a cocktail of certain bacteria, some of the areas of the
subjects’ brains were unmistakably altered, especially the areas
responsible for processing emotions and pain.
Of Irritated Bowels,
Stress, and Depression
NOT EVERY UNCHEWED pea can intervene in the brain’s activity.
A healthy gut does not transmit minor, unimportant digestive signals
to the brain via the vagus nerve. Rather, it processes them with its
own brain—that’s why it has one, after all. If it thinks something is
important, however, it may consider calling in the brain.
By the same token, the brain does not transfer every piece of
information to the conscious mind. If the vagus nerve wants to
deliver information to the extremely important locations in the brain, it
must get them past the doorman, so to speak. The brain’s bouncer is
the thalamus. When our eyes report to the thalamus for the twentieth
time that the same curtains are still hanging at the living-room
window, it refuses entry to that information—it is not important for the
conscious mind. A report of new living-room curtains is something it
would let in, for example. That is not true of everybody’s thalamus,
but most people’s.
An unchewed pea will not make it across the threshold from the
gut to the brain. The story is different for other stimuli, however. For
example, a report of an unusually large intake of alcohol will make it
from the belly to the head, where it informs the vomit control center;
information about trapped gas will reach the pain center; and the
presence of pathogenic substances will be reported to the officer in
charge of nausea. These stimuli make it through because the gut’s
threshold and the brain’s doorman consider them important. But it is
not only bad news that makes it across the border. Some signals can
cause us to fall asleep on the couch, contented and full after a big
Christmas dinner. We are conscious that some of these signals
originate from the belly; others are processed in the subconscious
areas of the brain and so cannot be located so clearly.
When a gut is irritated, its connection to the brain can make life
extremely unpleasant. This shows up on brain scans. In one
experiment, the activity in the brains of volunteers was imaged while
a small balloon was inflated inside their intestine. Healthy subjects
showed normal brain activity with no notable emotional components.
When patients with irritable bowels were subjected to the same
procedure, however, there were clear indications of activity in the
emotional center of the brain normally associated with unpleasant
feelings. So the stimulus was able to cross both barriers in those
subjects. The patients felt uneasy, although they had not endured
anything untoward.
Irritable bowel syndrome is often characterized by an unpleasant
bloated feeling or gurgling in the abdomen, and a susceptibility to
diarrhea or constipation. Sufferers also have an above-average
incidence of anxiety or depressive disorders. Experiments like the
one with the balloon show that feeling unwell and negative emotions
can arise via the gut–brain axis when the gut’s threshold is lowered
or when the brain insists on having information it would not normally
receive.
Such a state of affairs may be caused by tiny but persistent (socalled micro-) inflammations, bad gut flora, or undetected food
intolerances. Despite the wealth of recent research, some doctors
still dismiss patients with irritable bowel syndrome as
hypochondriacs or malingerers because their tests show no visible
damage to the gut.
Other diseases affecting the bowel are different. During an acute
phase of their condition, patients with a chronic inflammatory bowel
disease like Crohn’s disease or ulcerative colitis may have real sores
in their bowel wall. With these conditions the trouble is not that even
tiny stimuli are transferred from the gut to the brain—their threshold
is still high enough to prevent that. The problems are caused by the
diseased mucus membrane of the gut. Like patients with irritable
bowel syndrome, sufferers of these conditions also show increased
rates of depression and anxiety.
There are currently very few—but very good—research teams
studying how to make the threshold between the gut and the brain
less porous. This is important not only for patients with intestinal
problems, but for all of us. Stress is thought to be among the most
important stimuli discussed by the brain and the gut. When the brain
senses a major problem (such as time pressure or anger), it naturally
wants to solve it. To do so, it needs energy, which it borrows mainly
from the gut. The gut is informed of the emergency situation via the
sympathetic nerve fibers, and is instructed to obey the brain in this
exceptional period. It is kind enough to save energy on digestion,
producing less mucus and reducing the blood supply.
However, this system is not designed for long-term use. If the
brain permanently thinks it is in an emergency situation, it begins to
take undue advantage of the gut’s compliance. When that happens,
the gut is forced to send unpleasant signals to the brain to say it is
no longer willing to be exploited. This negative stimulus can cause
fatigue, loss of appetite, general malaise, or diarrhea. As with
emotional vomiting in response to upsetting situations, the gut reacts
by ridding itself of food to save energy so it is available to the brain.
The difference is that real stress situations can continue for much
longer than minor upsets. If the gut has to continue to forego energy
in favor of the brain, its health will eventually suffer. A reduced blood
supply and a thinner protective layer of mucus weaken the gut walls.
The immune cells that dwell in the gut wall begin to secrete large
amounts of signal substances, which make the gut brain increasingly
sensitive and lower the first threshold. Periods of stress mean the
brain borrows energy, and, as any housekeeper knows, good
budgeting is always better than running up too many debts.
One theory proposed by research bacteriologists is that stress is
unhygienic. The altered circumstances stress creates in the gut allow
different bacteria to survive there than in periods of low stress. We
could say stress changes the weather in the gut. Tough guys who
have no problem with turbulence will reproduce successfully—and at
the end of the day they are not likely to spread good cheer in the gut.
If this theory is true, that would make us not just the victims of our
own gut bacteria, but also the gardeners of our inner world. It would
also mean that our gut is capable of making us feel the negative
effects long after the period of stress is over.
Feelings from down below, especially those that leave a nasty
aftertaste, will cause the brain to think twice next time about whether
it really wants to hold a speech in front of the entire office, or whether
we really should eat that super-hot chili. So the process of making
decisions based on gut feeling may involve the gut recalling how it
felt in similar situations in the past. If positive lessons could also be
reinforced in the same manner, then the way to a lover’s heart really
would be through their stomach—and straight to the gut.
The interesting theory that our gut is not only involved in our
feelings and in making “gut decisions” but also may influence our
behavior is the subject of various research projects. A team at
McMaster University in Canada led by Stephen Collins designed an
ingenious experiment using two different strains of mice with very
well-researched behavioral characteristics. Members of the strain
called BALB/c are more timid and docile than those belonging to the
NIH Swiss strain, which exhibit more exploratory behavior and
gregariousness. The researchers gave the mice a cocktail of
antibiotics that affect only the gut, wiping out their entire gut flora.
They then fed the animals with gut bacteria typical of the other strain.
Behavior tests showed they had swapped roles—the BALB/c mice
became more gregarious and the NIH Swiss mice were more timid.
This shows that the gut can influence behavior—at least in mice. The
result cannot yet be applied to humans. Scientists know far too little
about the various bacteria involved, about the gut brain in general,
and about the gut–brain axis.
Until scientists have filled those gaps in their knowledge, we can
make use of the facts we already know to improve gut health. It
starts with the little things like mealtimes, for example, which should
be enjoyed without pressure, at a leisurely pace. The dinner table
should be a stress-free zone, with no place for scolding or
pronouncements like “You will remain at the table until you’ve
finished the food on your plate!” and without constant television
channel hopping. This is important for adults, but it is vital for small
children, whose gut brain develops in parallel with their head brain.
The earlier in life mealtime calm is introduced, the better. Stress of
any kind activates nerves that inhibit the digestive process, which
means we not only extract less energy from our food, we also take
longer to digest it, putting the gut under unnecessary extra strain.
We can play around with this knowledge and test it
experimentally. There are tablets and medicated chewing gum that
prevent travel sickness by numbing the nerves of the gut. When the
nausea abates, feelings of anxiety often disappear, too. If
unaccountable grumpiness or anxiety can originate in the gut (even
without nausea), is it possible that these drugs could be used to
banish them? By temporarily numbing a troubled gut, so to speak?
Alcohol reaches the nerves of the gut before it reaches those in the
brain—so how much of the relaxing effect of that “just one glass of
wine” in the evening actually comes from a sedated gut brain? What
about the array of bacteria in the wide range of yogurt on our
supermarket shelves? Is Lactobacillus reuteri better for me than
Bifidobacterium animalis? A team of Chinese researchers managed
to show in the laboratory that Lactobacillus reuteri is able to inhibit
pain sensors in the gut.
Lactobacillus plantarum and Bifidobacterium infantis could
already be recommended as a pain treatment for patients with
irritable bowel syndrome. Many patients with a low pain threshold in
the gut currently take substances designed to treat diarrhea,
constipation, or cramps. That might help with the symptoms, but it
does not address the cause of the problem. If, after eliminating
possible food intolerances and restocking the gut flora, there is still
no improvement, then we must take the problem by the scruff of its
neck—or in this case, by the nerve-cell threshold. So far, very few
treatments have been scientifically proven to be effective. One of
those is hypnotherapy.
Really good psychotherapy is like physiotherapy for the nerves. It
eases tensions and teaches us how to move in a more healthy way
—at the neural level. Because the nerves of the brain are more
complicated creatures than the muscles of the body, a trainer needs
to have more creative exercises up his sleeve. Hypnotherapists often
use thought journeys and guided imagery techniques. These aim to
reduce the intensity of pain signals and alter the way the brain
processes certain stimuli. Just like muscles, certain nerves can
become stronger with increased use. The therapy does not involve
hypnotism as seen in television shows. That would, in fact, be selfdefeating, since this kind of therapy relies on the patient being in
control at all times. Patients must make sure the hypnotherapist they
choose is recognized by a reputable institution.
Hypnotherapy has been shown to be effective in treating patients
with irritable bowel syndrome, reducing their reliance on medication
—in some cases to zero. This is particularly true of children with this
condition. For them, hypnotherapy has been shown to produce a 90percent reduction in pain, compared with a 40-percent reduction
produced by drugs. Some clinics offer specific hypnotherapy for
abdominal complaints.
Patients with intestinal disease who also suffer from extreme
anxiety or depressive disorders are often recommended
antidepressants by their doctor. However, they are rarely told why.
And there is a simple reason for that: no doctor or scientists knows.
It was not until they noticed the mood-enhancing effects of these
drugs that scientists began to explore the mechanisms behind this
phenomenon. They still have not come up with a clear answer. For
decades, it was thought to be due to an enhancing effect of the socalled happiness hormone serotonin. More recently, depression
researchers have also begun investigating another possibility—that
such drugs may increase the plasticity of the nerves.
Neuroplasticity is the nerves’ ability to change. It is nerve
plasticity that makes puberty such a confusing time for an adolescent
brain—so much is still being molded into shape. The possibilities are
endless and nerves are constantly firing off messages in all
directions in a pubescent brain. This process is not complete until we
reach the age of about twenty-five. After that, nerves react according
to well-rehearsed patterns. Patterns that have proved useful in the
past are retained; others are rejected as failures. This explains the
disappearance not only of the inexplicable fits of laughter and temper
tantrums of the teenage years, but also of the posters plastering the
bedroom walls. After this age, we find it more difficult to deal with
sudden change, but the payback is a more stable, calmer
disposition. This can also result in negative thought patterns taking
root, such as “I am worthless” or “Everything I do goes wrong.” The
nervous messages from a worried gut can also become embedded
in a person’s mind. If it is the case that antidepressants increase
neuroplasticity, they may work by loosening up such negative
thought patterns. This is most beneficial when accompanied by
effective psychotherapy to help patients resist slipping back into old
habits.
The side effects of commercially available antidepressants, such
as Prozac, also provide us with important clues about the so-called
happiness hormone serotonin. A quarter of patients report typical
side effects such as nausea, an initial phase of diarrhea, and
constipation when the drug is taken over a long period of time. This
is explained by the fact that our gut brain possesses the same neural
receptors as the brain in our head. So, antidepressants automatically
treat both brains. The American researcher Dr. Michael Gershon
takes this line of thought one stage further. He is interested in the
possibility of developing effective antidepressants that only influence
the gut and do not have an effect on the brain.
That is not as outlandish as it might first seem. After all, 95
percent of the serotonin we produce is manufactured in the cells of
our gut, where it has an enormous effect on enabling the nerves to
stimulate muscle movement and acts as an important signaling
molecule. If its effects on the gut can be changed, the messages
sent from there to the brain would also be changed enormously. This
would be particularly useful in treating the sudden onset of severe
depression in people whose lives are otherwise fine. Perhaps it is
their gut that needs a session on the therapist’s couch and their head
is not to blame at all.
Anyone who suffers from anxiety or depression should remember
that an unhappy gut can be the cause of an unhappy mind.
Sometimes, the gut has a perfect right to be unhappy—if it is dealing
with an undetected food intolerance, for example. We should not
always blame depression on the brain or on our life circumstances—
there is much more to us than that.
Where the Self Originates
well-being, and worry do not
originate in isolation in the mind. We are human beings, with arms
and legs, genitals, a heart, lungs, and a gut. Science’s concentration
on the brain has long blinded us to the fact that our self is made up
of more than just our gray matter. Recent gut research has
GRUMPINESS, HAPPINESS, INSECURITY,
contributed significantly to a new, cautious questioning of the
philosophical proposition “I think, therefore I am.”
One of the most fascinating parts of the brain that can receive
information from the gut is the insula, or insular cortex. This part of
the brain is studied by one of the most brilliant brains working in
research today: Bud Craig. With superhuman patience, he has spent
the last twenty years staining nerve fibers and tracking their paths
through the brain. Eventually, he emerged from the lab and gave a
one-hour talk revealing his theory that human self-awareness
originates in the insular cortex.
The first part of his hypothesis goes like this. The insula receives
information about feelings from the entire body. Each piece of
information is like a pixel. The insula then organizes these pixels to
form an overall image. This image is important because it represents
a map of our feelings. So, when we are sitting on a chair, we feel the
cheeks of our behind pressed against the seat, and we might also
feel cold or hungry, for example. Taken together, this gives the
overall picture of a cold, hungry person sitting on a hard chair. We
might not find this image particularly great, but it is also not awful—
it’s just okay.
Hypothesis, part two. Daniel Wolpert tells us the purpose of the
brain is to create movement—irrespective of whether you are a sea
squirt searching for a comfy rock beneath the sea or a human being
striving for the best life possible. The aim of movement is to bring
about an effect. The brain can use the insula’s map to plan
meaningful movement. If I am sitting around feeling cold and hungry,
other areas of the brain will be motivated to do something to change
my situation. I could start shivering, or I could get up and head for
the fridge in search of food. One of the main purposes of movement
is to shift us constantly toward a healthy equilibrium—from cold to
warm, from sad to happy, or from tired to alert, for example.
Hypothesis, part three. The brain is an organ of the body. So, if
the insula creates an image of the body, that image must also
include the on-board computer in our head. It has some interesting
areas, such as those responsible for social empathy, morality, and
logic. The social areas of the brain might give rise to negative
feelings when we argue with our partner; logic regions might induce
despair when we try to solve a difficult puzzle. In order for the insula
to create a reasonable image of our self, it probably also takes in
perceptions of our environment and experiences from the past. So,
when we are cold, we don’t just feel the low temperature, we are
able to contextualize the feeling and think such thoughts as “This is
weird. I’m cold, but I’m in a well-heated room indoors. Maybe I’m
coming down with something?” Or alternatively, “Okay, maybe I
shouldn’t be parading around naked in the conservatory in winter.” In
this way, humans are able to react to the stimulus of feeling cold in a
much more complex way than other animals.
The more information we connect, the cleverer the movements
we can make. In this respect, there is probably also a hierarchy
among our organs. Information that is particularly important for the
maintenance of a healthy equilibrium has more sway in the insula.
The brain and the gut are well qualified to take a central role—if not
the central role.
So, the insula creates a picture of our entire feeling body. We can
then use our complex brain to embellish this image. Bud Craig
believes the picture is refreshed approximately every forty seconds.
Through time, those images merge into a kind of movie—the film of
the self, of our life.
A great deal of what makes up this movie is certainly contributed
by the brain—but not everything. It may be time to expand René
Descartes’ proposition: “I feel, then I think, therefore I am.”
(PART THREE)
THE WORLD OF
MICROBES
LOOKING DOWN ON Earth from space, it is impossible to make out any
human beings. The Earth itself is easily identified—a bright, round
spot among the other bright spots in the darkness of space. Closing
in a little, it becomes apparent that we humans inhabit all sorts of
different places on the planet. Our cities shine at night as patches of
light. Some groups are concentrated in big urban centers, others live
scattered over wide areas. We inhabit the cool northern climes of
Europe and North America, but we also occupy tropical rainforests
and the margins of arid deserts. We are everywhere, even though
we are invisible from space.
Looking closer at human beings, it becomes clear that each of us
is a world of our own. Our forehead is a breezy meadow, our elbows
are arid wastelands, our eyes are salty lakes, and our gut is the most
amazing giant forest ever, populated by the weirdest of creatures.
Just as we humans occupy the planet, our bodies are occupied by a
population that reveals itself only under the microscope—bacteria.
Viewed at great magnification, they resemble bright, little spots
against a dark background.
For many centuries, humans concerned themselves with the
human-sized world. We measured it, examined its flora and fauna,
and philosophized about life. We constructed huge machines and
flew to the Moon. Explorers keen to discover new continents today
must turn to the microscopic world within us. Our gut is perhaps the
most fascinating continent of that world. It provides the habitat for
more species and families of creatures than any other landscape.
Exploration of this region is only now beginning in earnest. A new
sense of excitement is brewing among scientists, not unlike that
associated with the decoding of the human genome and all the
promise that holds for the future. Of course, this excitement about
gut research could still fizzle and come to nothing.
Work on an atlas of human bacteria did not begin until 2007. This
project involves taking cotton swab samples from all over the bodies
of lots and lots of people. Samples are collected from three different
areas of their mouths, under their armpits, and on their foreheads.
Stool samples are analyzed and genital smears are evaluated.
Places once thought to be bacteria-free turn out to be populated
after all—the lungs, for example. When it comes to drawing up a
bacteria atlas, the gut is the supreme challenge. Of our entire
microbiome—that is, all the microorganisms that teem on the inside
and outside of our bodies—99 percent are found in the gut. Not
because there are so few elsewhere, but because there are simply
so inconceivably many in the gut.
I Am an Ecosystem
WE ARE FAMILIAR with bacteria—those little creatures consisting of a
single cell. Some live in boiling hot springs in Iceland, while others
luxuriate in the moisture on a dog’s wet nose. Some require oxygen
to produce energy and “breathe” almost like us and others die when
exposed to the fresh air. Those who don’t draw their energy from
oxygen rely on metal atoms or acids—and that can result in some
rather interesting smells. Almost every body smell is, in fact,
produced by bacteria. From the pleasant scent of a loved one’s skin
to the dog-breath of next-door’s frisky hound—it is all the product of
the microscopic world in us, on us, and around us.
We like to watch athletic surfers as they ride the waves, but we
are unaware of the spectacular surfing scenario that takes place in
our nasal flora every time we sneeze. We pant and sweat when we
exercise, but no one notices how delighted the bacteria who live in
our running shoes are over the sudden, summery change in climate.
When we take a sneaky bite of cake, we never hear the roar of
excited bacteria in our gut, as they gleefully shout, “HERE COMES
CA-A-A-KE!” It would take an entire international news agency to
report on all the events constantly unfolding in just one person’s
microbiome. While we lounge about feeling bored, any number of
exciting things are happening inside us.
People are slowly beginning to realize that the vast majority of
bacteria are harmless, or even helpful. Some facts are now known to
science. Our gut’s microbiome can weigh up to 4½ pounds (2 kilos)
and contains about 100 trillion bacteria. One-thirty-second of an
ounce (1 gram) of feces contains more bacteria than there are
people on Earth. We also know that this community of microbes
cracks open indigestible foodstuffs for us, supplies the gut with
energy, manufactures vitamins, breaks down toxins and medications,
and trains our immune system. Different bacteria manufacture
different substances: acids, gases, fats. You could say bacteria are
tiny factories. We know that gut bacteria are responsible for blood
groups and that harmful bacteria cause diarrhea.
What we don’t know is what all this means for each individual.
We notice pretty quickly when we have ingested diarrhea-causing
bacteria. But what do we notice of the work carried out by the many
millions, billions, trillions of tiny creatures inside us every day? Does
the precise nature of the creatures that colonize us make a
difference? Skewed proportions of the different bacteria in our gut
have been detected in those suffering from obesity, malnutrition,
nervous diseases, depression, and chronic digestive problems. In
other words, when something is wrong with our microbiome,
something goes wrong with us.
One person might have stronger nerves than another because
she has a better stock of vitamin B–producing bacteria. Another
person might be able to deal easily with bit of bread mold eaten by
mistake. Yet another might have a tendency to gain weight because
the “chubby” bacteria in his gut feed him a bit too willingly. Science is
just beginning to understand that each of us is an entire ecosystem.
Microbiome research is still young, complete with wobbly milk teeth
and short pants.
Bacteria population density in the different regions of the gut.
When scientists still knew very little about bacteria, they classified
them as plants. This explains terms like gut flora, which is not
scientifically accurate, but it is appropriately descriptive. A bit like
plants, different bacteria have different characteristics concerning
their habitat, nutrition, or level of toxicity. The scientifically correct
terms are microbiota (which means “little life”) and microbiome, to
refer to our collection of microbes and their genes.
In general, it is accurate to say that the number of bacteria is
smaller in the upper sections of the digestive tract, while a very, very
large number reside in the lower parts, such as the large intestine
and the rectum. Some bacteria prefer the small intestine; others live
exclusively in the colon. There are great fans of the appendix, wellbehaved homebodies that stick to the mucus membrane, and rather
cheekier chaps that nestle up close to the cells of our gut.
It is not always easy to get to know our gut microbes personally.
They don’t like to be removed from their own world. When scientists
try to grow them in the lab to observe them, they simply refuse to
cooperate. Skin bacteria merrily gobble up the lab food and grow into
little microbe mountains—gut bacteria don’t. More than half the
bacteria that grow in our digestive tract are just too well adapted to
living there to be able to survive outside the gut. Our gut is their
world. It keeps them warm, moist, protected from oxygen, and
supplied with pretasted food.
Only ten years ago, many scientists would probably have
maintained that there is a stable stock of gut bacteria that is more or
less common to every human being. For example, when they spread
feces on a culture medium, they always found E. coli bacteria. It was
as simple as that. Today, we have machines that can scan tiny
amounts of feces molecule by molecule. This reveals the genetic
remains of billions of bacteria. We now know that E. coli make up
less than 1 percent of the population in the gut. Our gastrointestinal
tract is home to more than a thousand different species of bacteria—
plus minority populations of viruses and yeasts, as well as fungi and
various other single-celled organisms.
You might think our immune system would pounce on this
multitude of settlers. Defending the body from foreign invasions is
high on the immune system’s to-do list. Sometimes it even wages
war on tiny pollen grains that accidently get sucked into our nostrils.
Hay fever sufferers know the signs: a streaming nose and itchy eyes.
So, how do the bacteria sidestep the immune system and stage a
bacterial Woodstock inside our bodies?
The Immune System and Our Bacteria
WE FACE POTENTIAL death every day. We could get cancer, get eaten
away by bacteria, or get infected with a deadly virus. And several
times a day, our lives are saved. Strangely mutated cells are
destroyed, fungal spores are eliminated, bacteria are peppered with
holes, and viruses are sliced in two. This agreeable service is
provided by our immune system, with its many little cells. Its
workforce includes experts at spotting foreign bodies, contract killers,
hatters, and mediators. They all work hand in hand, and together
they are a pretty top team.
The vast majority of our immune system (about 80 percent) is
located in the gut. And with good reason. This is where the main
stage at the bacterial Woodstock is situated, and any immune
system worth its salt must be there or be square. The bacteria are
confined to a fenced-off area—the mucus membrane of the gut—
preventing them from getting too dangerously close to the cells of
the gut wall. The immune system can play with the cells without ever
posing a danger to the body. This allows our defender cells to get
acquainted with many previously unknown species.
If, sometime later and elsewhere in the body, an immune cell
encounters a now-familiar bacterium, it can react to it much more
quickly. The immune system has to be extremely careful in the gut,
suppressing its defensive instincts and allowing the many bacteria
there to live in peace. But, at the same time, it must also recognize
dangerous elements in the crowd and weed them out. If we decided
to say “Hi” to each of our gut bacteria individually, we might just
manage it in around 3 million years. Our immune system not only
says, “Hi,” it also says, “You’re okay,” or “I’d prefer to see you dead.”
Also, strange as it may sound, the immune system must be able
to distinguish between bacterial cells and the body’s own human
cells. That is easier said than done. Some bacteria have structures
on their surface that bear a close resemblance to those on the
surface of our own cells. This is the reason why, for example, scarlet
fever should be treated immediately with antibiotics. If it is not
treated quickly, the immune system can begin to mistake the cells of
the joints or other organs for the bacteria that cause scarlet fever
and attack them. It might suddenly think our knee is a nasty sorethroat germ hiding out in our leg. It happens rarely—but it does
happen.
Scientists have observed a similar effect in patients with juvenile
diabetes. Also called diabetes mellitus type 1, this condition results
from the autoimmune destruction of the cells that produce insulin.
One possible cause is a breakdown of communication with the
bacteria of the gut. It may be that they are failing to train the immune
system properly or the immune system is somehow getting the
message wrong.
The body actually has a very rigorous set of measures designed
to guard against such communication breakdowns and cases of
mistaken identity. Before an immune cell is allowed to enter the
bloodstream, it has to complete the toughest boot camp of any cells.
Among other things, it must cover a vast distance while being
constantly confronted with various structures of the body. If our little
immune cell encounters something it cannot clearly identify as
belonging to the body or coming from outside, it stops and prods at it
a little. That is a fatal error: this cell will never graduate to the
bloodstream.
In this way, immune cells with a tendency to attack the body’s
own tissue are weeded out before they leave boot camp. In their
training center in the gut, they learn to be tolerant of foreign bodies,
or rather, they learn to be better prepared for an encounter with
them. This system works rather well and usually without untoward
incidents.
There is one lesson that is particularly tricky to learn: what to do
about foreign bodies that aren’t actually bacteria but remind the
immune system of them? Red blood cells, for example, have very
bacteria-like proteins on their surface. Our immune system would
attack our own blood if it had not learned in boot camp that the blood
is a no-go area. If our blood cells have the blood-group marker A on
their surface, we have no problem receiving transfusions of blood
from donors with the same blood group. The reasons for needing a
transfusion can be diverse, from a motorbike accident to heavy blood
loss during childbirth.
However, we cannot receive blood from donors whose blood cells
have a different blood-group marker on their surface. It would
immediately remind our immune system of bacteria, and since the
immune system knows that bacteria have no business being in the
bloodstream, it would consider the donated blood cells an enemy
and cause the cells to form clumps. If it weren’t for this combat
readiness—learned through training by our gut bacteria—there
would be no blood groups and any donor could give blood to any
recipient. For newborn babies, who do not yet have many bacteria in
their guts, this is indeed the case. They can theoretically receive
transfusions of blood from any group without any incompatibility
effects. (As a precaution, hospitals give babies blood from the
mother’s blood group, since antibodies from the mother can find their
way into the baby’s bloodstream.) As soon as babies begin to
develop a rudimentary immune system and gut flora, they can only
tolerate blood from their own group.
If antibodies match with foreign blood cells, the cells will form clumps. Blood group B has
antibodies against blood group A.
Blood-group development is just one of many immunological
phenomena caused by bacteria. There are probably many more
waiting to be discovered. Much of what bacteria do tends to be fine
tuning. Each kind of bacteria has its own way of affecting the
immune system. Some species have been observed to make our
immune system more tolerant, for example, by causing more peaceloving, mediatory immune cells to be produced, or by affecting our
cells in a similar way to cortisone and other anti-inflammatory drugs.
That results in a milder, less belligerent immune system. This is
probably a clever move on the part of these tiny creatures, since it
increases their chances of being tolerated in the gut.
The fact that the small intestines of young vertebrates (including
humans) have been found to contain bacteria that provoke the
immune system leaves room for speculation. Could it be the case
that these provocateurs help keep the bacteria population in the
small intestine down? That would make the small intestine an area of
low bacteria tolerance, giving it some peace and quiet for a while.
The provocateurs themselves do not hang out in the mucus
membrane like good little bacteria, but dock firmly onto the villi of the
small intestine. A similar preference is shown by pathogens such as
harmful versions of E. coli. When they want to colonize the small
intestine, but find their favorite places occupied by such
provocateurs, they have no choice but to leave.
This effect is known as colonization resistance. The majority of
the microbes in our gut protect us simply by occupying spaces that
would otherwise be free for harmful bacteria to colonize. Incidentally,
the provocateurs of the small intestine belong to that group of
characters that refuse to be cultivated outside the gut. How can we
be sure that they are not actually harming us? Well, we can’t. It is
possible that they do harm some people by overstimulating the
immune system. Many questions remain to be answered.
Some of those questions might be answered with the help of a
group of germ-free mice in a New York laboratory. They are the
cleanest creatures in the world: they come into the world via sterile
cesarean births, they live in antiseptic cages, and they eat steamsterilized food. Disinfected animals like these could never exist in
nature. Anyone working with these mice must take the utmost care,
since even unfiltered air teems with flying germs. The mice allow
researchers to watch what happens to an immune system that has
nothing to do. What goes on in a gut with no microbes? How does an
untrained immune system react to pathogens? What differences are
so obvious they can be seen by the naked eye?
Anyone who has ever had anything to do with such animals will
tell you—germ-free mice are weird. They are often hyperactive and
exhibit an un-mouse-like lack of caution. They eat more than their
germ-colonized peers and take longer to digest their food. They have
hugely enlarged appendixes, shriveled digestive tracts with few villi
and blood vessels, and a reduced number of immune cells. They are
easy prey for even relatively harmless pathogens.
Feeding them with cocktails of bacteria taken from other mice
produces astonishing results. If they are given bacteria from mice
with type 2 diabetes, they soon begin to develop problems
metabolizing sugar. If bacteria from obese humans are fed to germfree mice, the mice are more likely to gain weight than if they receive
bacteria from people in the normal weight range. Scientists can also
administer a single species of bacteria to observe its effect on the
mice. Some bacteria, acting alone, can reverse the effects of the
sterile environment—cranking up the immune system, shrinking the
mice’s swollen appendixes down to normal size, and normalizing
their eating behavior. Other lone bacteria have no effect whatsoever.
Yet others take effect only in cooperation with colleagues from other
bacteria families.
Studies using these mice have advanced our knowledge quite
considerably. We now have good reason to speculate that, just as
the macroscopic world we live in influences us, we are also
influenced by the microscopic world that lives in us. This is all the
more interesting when we realize that each person’s inner world is
unique to him or her.
The Development of the Gut Flora
AS UNBORN BABIES, we live in an environment that is normally
completely germ-free—the womb. For nine months, we have no
contact with the outside world except through our mother. Our food is
predigested, our oxygen is prebreathed. Our mother’s lungs and gut
filter everything before it reaches us. We eat and breathe through her
blood, which is kept free of germs by her immune system. We are
sheathed in an amniotic sac and encased in a muscly uterus that is
corked with a thick plug like a big earthenware jug. All this means not
a single parasite, virus, bacterium, or fungus—and certainly no other
person—can touch us. We are more sterile than an operating table
flooded with disinfectant.
This situation is unusual. Never again in our lives will we be so
protected and so isolated. If we were designed to remain germ-free
once we leave the womb, we would be very different creatures. But
that is not the case, so all living things of any size have at least one
other living thing that helps them in some way and is allowed to live
on or in them in return. This explains why our cells are constructed in
such a way that bacteria can easily dock with structures on their
surface, and it explains why certain bacteria have coevolved with us
over many millennia.
As soon as there is any breach in the protective amniotic sac,
colonization begins. While 100 percent of the cells that make us up
when we start life are human cells, we are soon colonized by so
many microorganisms that only 10 percent of our cells are human,
with microbes accounting for the remaining 90 percent. We cannot
see this, because our human cells are so much larger than those of
our new lodgers. Before we look into our mother’s eyes for the first
time, the creatures that live in her body cavities have already looked
into ours. The first ones we meet are her protective vaginal flora—an
army that defends a very important territory. One way it does this is
by producing acids that drive away other bacteria and keep the way
cleaner and cleaner the closer they are to the womb.
Unlike the flora in our nostrils, which can be made up of around
nine hundred different kinds of bacteria, the criteria for life in the birth
canal are much stricter. This sorting process leaves women with a
useful coating of bacteria, which wraps itself protectively around the
sterile body of the baby as it emerges. About half these bacteria are
from one genus: Lactobacillus. Their favorite pastime is producing
lactic acid. This means the only residents that can set up home in
the birth canal are those that pass the acid test.
With a routine birth, all we have to do as babies is decide which
way to face as we come out. There are two attractive possibilities:
toward the back or toward the front. During birth we are exposed to
all sorts of skin contact before we are wrapped up in something soft
by another person, who is usually wearing latex gloves.
By now, the founding fathers of our first microbial colonies are
already in us and on us. These are mainly our mother’s vaginal and
gut flora, mixed with a few skin-dwelling germs and possibly a few
others from the hospital’s repertoire. This is a very good mixture to
start with. The acid army protects us from harmful invaders, while
other bacteria are already starting to train the immune system, and
the first, indigestible components of our mother’s milk are broken
down for us by helpful microbes.
Some of these bacteria take less than twenty minutes to spawn
the next generation. What takes us twenty years or more happens in
a fraction of the time—a fraction as tiny as the colonists themselves.
While our first gut bacterium watches its great-great-great-great
grandchild swim by, we have spent just two hours in the arms of our
proud new parents.
Despite this rapid population growth, it will be about three years
before the gut flora develops to the right level and then stabilizes.
Prior to that, our gut is the scene of dramatic power struggles and
great bacterial battles. Some folks who find their way into our mouth
spread rapidly throughout the gut, only to disappear again just as
quickly. Others will remain with us for the rest of our lives. The
composition of our gut colony depends partly on our own actions: we
might lick our mother’s skin, gnaw on a chair leg, and give the car
window or the neighbor’s dog the occasional sloppy kiss. Anything
that finds its way into our mouth in the process could soon be
building its empire in the world of our gut. Whether it will continue to
prevail will remain to be seen. And whether its intentions are good or
bad will also remain to be seen. So, we could say we gather our own
fate with our mouth. Stool samples can show what comes out the
other end. It’s a game with many unknowns.
We receive some help creating this collection—mainly from our
mother. No matter how many sloppy kisses we give to the car
window, if we are allowed to kiss and cuddle with our mother
regularly, we will be protected by her microbes. Breast-feeding also
promotes particular members of our gut flora—breast-milk-loving
Bifidobacteria, for example. Colonizing the gut so early, these
bacteria are instrumental in the development of later bodily functions,
such as those of the immune system or the metabolic system.
Children with insufficient Bifidobacteria in their gut in their first year
have an increased risk of obesity in later life compared with infants
with large populations.
There are many, many kinds of bacteria—some beneficial, others
less so. Breast-feeding can help shift the balance toward the
beneficial and reduce the risk of a later gluten intolerance, for
example. A baby’s first population of gut bacteria prepares the way
for the mature population by removing oxygen and electrons from
the intestine. As soon as the environment is free of oxygen, the more
typical bacteria of the gut can start to settle there.
Breast milk is so beneficial that a more or less well-nourished
mother need not do any more than suckle her baby to ensure it is
receiving a healthy diet. When it comes to the nutrients it contains,
breast milk provides everything that dietary scientists believe
children need in order to thrive—it is the best dietary supplement
ever. It contains everything, knows everything, and can do
everything necessary for a child’s well-being. And, as if that weren’t
enough, it has the added advantage of passing on a bit of Mom’s
immune system to her offspring. Breast milk contains antibodies that
can protect against any dangerous bacteria a child might make the
acquaintance of (by licking the family pet, for example).
Weaning is the first revolution experienced by a baby’s gut flora.
Suddenly, the entire composition of Junior’s food supply is different.
Clever old Mother Nature has equipped the typical bacteria that first
colonize the infant gut with the genes needed to break down simple
carbohydrates such as those in rice. Serve Junior complex, plantbased foods like garden peas, for example, and his baby flora will
not be able to deal with them alone. He is now going to need new
kinds of digestive bacteria. African children have bacteria that can
manufacture all kinds of tools needed to break down even the most
fibrous of plant-based foods. The microbes in the guts of children
with a Western diet prefer to avoid such hard work—and they may
do so with a clear conscience since their diet consists primarily of
puréed baby food and small amounts of meat.
Bacteria do not always manufacture the tools they need—
sometimes they also borrow them. In Japan, the gut population has
entered into a trade relationship with marine bacteria. They borrowed
a gene from their sea-living colleagues that helps break down the
kind of seaweed used in Japanese cuisine to make sushi, for
example. This shows that the composition of our gut population can
depend to a large extent on the tools we need to break down certain
foodstuffs.
Useful gut bacteria can be passed on through the generations.
Anyone of European heritage who has experienced constipation
after a blow-out session at the all-you-can-eat sushi bar will
appreciate the advantage of inheriting Japanese seaweedprocessing bacteria from someone in the family. However, it is not so
easy to infuse yourself or your kids with a few sushi-digesting
assistants. Bacteria have to like living in the place where they work.
If we say a microorganism is particularly suited to our gut, we
mean it appreciates the architecture of our gut cells, copes well with
the climate, and likes the food on the menu. All three of these factors
vary from person to person. Our genes help design our bodies, but
they are not the chief architects of our microbial home. Identical
twins share the same genes, but they do not have the same bacterial
mix. They do not even have noticeably more similarities than other
pairs of siblings. Our life-style, random acquaintances, illness, or
hobbies all influence the shape of the populations inside our body.
On the way to a relatively mature gut flora in our third year, we
stick all sorts of stuff into our mouth—some of which will be useful
and suited to us. We acquire more and more microorganisms,
building up our population diversity from a couple of hundred species
of bacteria to many hundreds of different gut-dwellers. That would be
a pretty impressive inventory for any zoo, yet we acquire this variety
without even thinking about it.
It is now generally accepted that the first populations to colonize
our gut lay the main foundations for the future of our entire body.
Studies have shown the importance of those first few weeks of
postnatal bacteria-collecting for the development of the immune
system. Just three weeks after birth, the metabolic products of our
gut flora can predict increased risks of allergies, asthma, or
neurodermatitis in later life. How do we manage to pick up bacteria
that are more harmful than beneficial to us so early in life?
More than a third of all children in Western, industrialized
countries are brought into the world by means of a convenient
cesarean section. No squeezing through a narrow birth canal, no
unpleasant side effects like perineal tearing, no delivering the
afterbirth—it sounds like a fine thing. The initial contact experienced
by children born by cesarean section is mainly with other people’s
skin. They have to glean bacteria for their gut somehow, since their
population will not develop from maternal microbes, like those of
children born vaginally. They might end up with bacteria from Nurse
Suzy’s right thumb, from the florist who sold Daddy that
congratulatory bunch of flowers, or from Granddad’s dog. Suddenly,
factors like the motivation of underpaid hospital cleaners become
significant. Did they wipe down the telephones, tables, and bathroom
faucets with loving care or a lack of conviction?
Our skin flora is not as strictly controlled as that of the birth canal
and is much more exposed to the outside world. Whatever gathers
on the skin could soon end up in baby’s belly. These uninvited
guests may include pathogens or weird types with strange ways of
training the young immune system. Children born by cesarean
section take months or even longer to develop a normal population
of gut bacteria. Three-quarters of newborn babies who pick up
typical hospital germs are those born by cesarean section. They also
have an increased risk of developing allergies or asthma. One
American study showed that administering Lactobacillus to those
babies can reduce their risk of developing allergies. The same
treatment has no effect at all on children born naturally—one could
say they were dipped in the probiotic waters of the Styx while they
were being born.
By the age of seven, there is barely any discernible difference
between the gut flora of children born naturally and those born by
cesarean section—the early stages, when the immune and
metabolic systems are still impressionable, are long gone. Indeed,
cesarean births are not the exclusive cause of less-than-ideal
starting populations in the gut. Poor nutrition, unnecessary use of
antibiotics, excessive cleanliness, or too much exposure to bad
bacteria can also feature among the causes. In spite of all this, there
is no reason for anyone to feel inadequate. We humans are large
creatures, and there is no way we can exercise control over every
aspect of our microscopic world.
The Adult Gut Population
IN TERMS OF our microbiota, we reach adulthood around the age of
three. For a gut, being an adult means knowing how you work and
what you like. When that stage has been reached, some gut
microbes find themselves on a great expedition with us through our
entire lives. We dictate the itinerary—by eating what we eat, reacting
to stress, going through puberty, getting ill, and growing old.
Those people who post pictures of their dinner on Facebook, only
to be disappointed by the lack of “likes” from friends, are simply
trying to appeal to the wrong audience. If there were such a thing as
Facebug (Facebook for microbes!), a picture of your dinner would
provoke an excited response from millions of users—and shudders
of disgust from millions more. The menu changes daily: useful milk
digesters contained in a cheese sandwich, armies of Salmonella
bacteria hiding in a delicious dish of tiramisu. Sometimes we alter
our gut flora, and sometimes it alters us. We are our flora’s weather
and its seasons. Our flora can take care of us, or it can poison us.
We are only now beginning to learn the impact the gut-based
bacterial community can have on an adult human. In this respect,
scientists know more about bees than about human beings. For
bees, having more diverse gut bacteria has been a more successful
evolutionary strategy. They were only able to evolve from their
carnivorous wasp ancestors because they picked up new kinds of
gut microbes that were able to extract energy from plant pollen. That
allowed bees to become vegetarians. Beneficial bacteria provide
bees with an insurance policy in times of food scarcity: they have no
trouble digesting unfamiliar nectar from far-flung fields. More
specialized digesters are not so well equipped. Times of crisis
highlight the advantage of hosting a good microbial army. Bees with
well-equipped gut flora can deal with parasite attacks better than
those without. Gut bacteria are an incredibly important factor in this
evolutionary survival strategy.
Unfortunately, we cannot simply transfer these results to humans.
Humans are not bees; they are vertebrates and they use Facebook.
So researchers have to go back to square one. Scientists
investigating our gut bacteria have to learn to understand an almost
completely unknown world and its interaction with the world outside.
First, they need to know who is living inside our gut.
So let’s take a closer look. Who exactly are these characters?
Biologists love to put things in order—from the contents of their
own desks to the entire contents of the world. They begin by sorting
everything into two large drawers: one for living things and the other
for non-living things. They then go on to divide everything in the first
drawer into three categories: eukaryotes, Archaea, and bacteria.
Representatives of all three groups can be found in the gut. I am not
promising too much when I say each of the three groups has its own
kind of charm.
Eukaryotes are made up of the largest and most complex cells.
They can be multicellular and grow to a pretty impressive size. A
whale is a eukaryote. Humans are eukaryotes. Ants are too,
incidentally, although they are much smaller than we are. Modern
biologists divide eukaryotes into six subgroups: crawly amoeboid
microbes, microbes with pseudopodia (foot-like protrusions that
aren’t real feet), plant-like organisms, single-celled organisms with
little mouth-like feeding grooves, algae, and opisthokonts.
For those unfamiliar with the term opisthokont (it comes from the
Greek words for “rear” and “pole”), it describes the group that
includes all animals—humans as well—and also fungi. So, the next
time you meet an ant in the street you can give it a friendly wave as
a fellow opisthokont. The most common eukaryotes found in the gut
are yeasts, which are also opisthokonts. We are familiar with yeast
as a rising agent for bread, but there are many other kinds.
Archaea are kind of in-betweeners. Not really eukaryotes, but not
really bacteria, either. Their cells are small and complex. If this
description seems a little vague, it may help if I say that the Archaea
are pretty rad characters. They love the extreme things in life. Some
are hyperthermophiles, which feel right at home in temperatures of
more than 212 degrees Fahrenheit (100 degrees Celsius) and are
often to be found hanging out near volcanoes. The acidophiles
among the Archaea like to paddle around in highly concentrated
acid. Barophiles (also called piezophiles) thrive under pressure and
have specially adapted cell walls to allow them to live on the deep
sea floor. Halophiles are at home in extremely salty water (they love
the Dead Sea). The rare characters among the Archaea that can be
cultured in the lab are the cryophiles, which love the cold. They like
laboratory freezers that keep them at a cozy minus 112 degrees
Fahrenheit (minus 80 degrees Celsius). There is one species of
Archaea often found in our gut that thrives on the waste products of
other gut bacteria and can glow.
Returning to the main topic: bacteria make up more than 90
percent of the population of our gut. Biologists divide bacteria into
more than twenty phyla or lineages. Members of different phyla are
sometimes about as similar as human beings are to excavates
(single-cell microbes with feeding grooves)—that is to say, not very.
Most of the inhabitants of our gut belong to one of five phyla: mainly
Bacteroidetes and Firmicutes, with a smattering of Actinobacteria,
Proteobacteria, and Verrucomicrobia. These phyla are further
divided into increasingly specific categories, until we eventually
reach the level of the bacteria family. Members of a given family are
relatively similar to each other. They eat the same food, keep similar
company, and have similar abilities. Individual family members have
impressive names like Bacteroides uniformis, Lactobacillus
acidophilus, or Helicobacter pylori. The bacteria kingdom is huge.
Whenever scientists search humans for a particular bacterium,
they constantly come across new, previously unknown species. Or
they discover known species in unexpected places. In 2011, a group
of researchers in the United States decided to examine the flora of
volunteers’ belly buttons, just for fun. One subject’s navel was found
to contain bacteria that were previously known to live only in the
seas off the coast of Japan—despite the fact that the volunteer had
never even been to Asia. Globalization is not just your local corner
shop turning into a McDonald’s—it affects even the contents of our
navels. Every day, billions and billions of foreign microorganisms fly
round the world without paying a single cent for their tickets.
Everyone has their own personal collection of bacteria. It could
even be described as a unique bacterial fingerprint. If you were to
take swabs from a dog and analyze the genes of its bacteria, the
dog’s owner could be easily identified with reasonable certainty. The
same is true of computer keyboards. Anything we come into regular
contact with carries our microbial signature. Everyone has some
outlandish items in their collection that almost no one else will share.
Rough overview of the three most important phyla of bacteria and their subgroups.
Lactobacilli are Firmicutes, for example.
The microbial landscape in our gut is just as unique and
individual. So, how are doctors supposed to know what is beneficial
and what is harmful? Uniqueness like this presents researchers with
a problem. If they are trying to ascertain what influence our gut
bacteria have on our health, it is no use finding out that Mr. Smith is
carrying a strange Asian species and several other weird microbes in
his gut. Scientists need to identify patterns to deduce facts from
them.
So, since scientists are faced with more than a thousand different
families of bacteria, they must decide whether they need to identify
just rough lineages or whether they should look at every paid-up
member of the Bacteroides bacteria family individually. E. coli and its
evil twin EHEC are members of the same family, for example. The
differences between them are infinitesimally small—but they are very
tangible: E. coli is a harmless gut-dweller, while EHEC causes severe
internal bleeding and diarrhea. It always makes sense to examine
families or lineages when you want to know what damage individual
bacteria can wreak.
The Genes of Our Bacteria
Genes are information. Genes can be
dominant, forcing features on us, or they can just offer their abilities
for us to use or not. But most of all, genes are plans. They are
incapable of doing anything unless they are read and implemented.
Implementation of some of these plans is obligatory—they decide
whether we are a human being or a bacterium, for example. Others
(say, liver spots) can be left on the back burner for years and yet
others might be carried for a lifetime without ever being expressed—
GENES ARE POSSIBILITIES.
for example, genes for large breasts. Some people might consider
that a pity, others a blessing.
Taken together, our gut bacteria have 150 times more genes than
a human being. This massive collection of genes is called a biome. If
we could pick 150 different living things, parts of whose genetic
blueprints we would like to possess, what would we choose? Some
people might opt for the strength of a lion, the wings of a bird, the
hearing of a bat, or the practical mobile home of a snail.
There are many reasons why it would be more practical to opt for
bacterial genes instead. They can be taken in easily via the mouth,
unfurl their abilities in the gut, and even adapt to our lifestyle.
Nobody needs a snail’s mobile home all the time, and no one needs
breast-milk-digestion helpers forever. The latter disappear gradually
after weaning. It is not yet possible to examine all the genes of our
gut bacteria at once. However, it is possible to search specifically for
individual genes, if you know what you are looking for. We know that
babies contain more active genes for digesting breast milk than
adults do. The guts of obese people are often found to contain more
bacterial genes involved in breaking down carbohydrates. Older
people have fewer bacterial genes for dealing with stress. In Tokyo,
gut bacteria can help digest seaweed, and in Toronto, they probably
can’t. Our gut bacteria paint a rough portrait of who we are: young,
chubby, or Asian, perhaps.
The genes of our gut bacteria also inform us about our body’s
abilities. The pain-relief drug acetaminophen can be more toxic for
some people than others: some gut bacteria produce a substance
that influences the liver’s ability to detoxify the drug. Whether you
can pop a pill to cure your headache without a second thought is
decided partially in your gut.
Similar caution should be exercised with general dietary tips.
Soy’s ability to protect against prostate cancer, cardiovascular
disease, or bone disorders, for example, has now been proven. More
than 50 percent of Asians benefit from this effect. Among people of
European heritage, the beneficial effect is found among only 25 to 30
percent of the population. This cannot simply be explained by human
genetic differences. The difference is due to certain bacteria. They
are found more commonly in the guts of Asians, where they are able
to coax the health-promoting essence out of tofu and other soy
products.
It is great for science when it identifies the individual bacterial
genes that are responsible for this beneficial effect. In such cases,
science can be said to have come up with an answer to the question
of how gut bacteria influence our health. But we want more than that.
We want to understand the big picture. If you look at all the bacterial
genes so far discovered, the small individual groups of genes
responsible for breaking down painkillers or soy products fade into
the background. The common features they share dominate the
picture. Every microbe contains many genes involved in breaking
down carbohydrates or proteins and in producing vitamins.
Science has the same problem when investigating the
microbiome that the Google generation regularly faces. We ask a
question and six million sources send us simultaneous answers. We
don’t respond by telling them to form an orderly line. We have to sort
them shrewdly into categories, weed out the irrelevant ones, and
recognize important patterns. One important step in this direction
was the discovery of the three human enterotypes in 2011.
Researchers in Heidelberg, Germany, were using cutting-edge
technology to investigate the human gut biome. They expected to
see the usual picture: a chaotic mixture of many different bacteria,
including a host of unknown species. What they actually discovered
came as a surprise. Despite the great diversity, there was order. One
of three families was always dominant in the realm of bacteria.
Suddenly, the whole mess of more than a thousand families looked
much more organized.
The Three Gut Types
depends on the family of bacteria that
dominates the microbe population of their gut. The choice is between
families that bask in the glory of the names Bacteroides, Prevotella,
and Ruminococcus. Researchers identified these enterotypes
distributed among Asians, Americans, and Europeans, irrespective
of age or gender. In the future, enterotyping may help doctors predict
a whole range of characteristics, such as the body’s response to soy,
nerve resilience, or susceptibility to certain diseases.
Practitioners of traditional Chinese medicine who were visiting
the institute in Heidelberg at the time of this discovery recognized an
opportunity to combine their ancient knowledge with modern
medicine. Classical Chinese medical theory has always divided
people into three groups according to how they react to certain
medicinal plants, such as ginger. The families of bacteria in our
bodies also have different characteristics. They break down food in
different ways, produce different substances, and detoxify certain
toxins but not others. Furthermore, they may also influence the gut
flora by either encouraging or attacking bacteria from the other two
groups.
A PERSON’S ENTEROTYPE
Bacteroides
Bacteroides ARE THE best-known family of gut bacteria and often form
the dominant population. They are experts in breaking down
carbohydrates, and they possess a huge collection of genetic
blueprints, which allows them to manufacture any enzyme they need
to accomplish that task. Whether we eat a steak, munch a large
salad, or chew on a raffia doormat in a drunken stupor, Bacteroides
know straight away which enzymes they need. They are equipped to
extract energy from whatever we ingest.
Their ability to extract the maximum energy from everything and
pass it on to us has led to the suspicion that they may be responsible
for an increased tendency to gain weight. Indeed, Bacteroides do
seem to like meat and saturated fatty acids. They are more common
in the guts of people who eat plenty of sausages and the like. But,
does having them in our gut make us fat, or does being fat lead to
having them in our gut? This question remains to be answered.
Bacteroides carriers are also likely to have a weakness for their
colleagues, Parabacteroides. These bacteria are also particularly
deft at passing on as many calories to us as possible.
This enterotype is also notable, among other things, for its ability
to produce particularly large amounts of biotin. Other terms for biotin
include vitamin B7 and vitamin H. It was given the name vitamin H in
the 1930s because of its ability to heal a certain skin condition
caused by consuming too much raw egg white. “H is for healing”
might not be the most creative mnemonic, but it is a useful one
nonetheless.
Vitamin H neutralizes avidin, a toxin found in raw eggs. It causes
the skin disease in question by binding strongly with vitamin H,
leaving the body deficient in that substance. So, eating raw eggs
causes vitamin H deficiency, which in turn can lead to skin disease.
I do not know who was eating enough raw eggs in the 1930s to
lead to the discovery of this connection. I do, however, know who
might possibly end up eating so much avidin in the future that they
could have problems with vitamin H—pigs who accidently roam into
a field of genetically modified corn. Genetic engineers have created
transgenic corn with a gene that produces avidin to make it less
susceptible to insect damage during storage. When pests—or stray
pigs—consume the corn, they are poisoned. When the corn is
cooked, it is no longer toxic, just like a good hard-boiled egg.
Another indication that our gut microbes produce vitamin H is the
fact that some people excrete more of it than they take in. Since no
human cell is capable of producing this substance, the only possible
explanation for this is that our bacteria are functioning as hidden
vitamin H factories. Vitamin H is not only necessary for “healthylooking skin, shiny hair, and strong nails,” as you might read on the
packages of supplements you can buy in your local pharmacy. Biotin
is also involved in some of the body’s vital metabolic processes. We
need it to synthesize carbohydrates and fats for our body, and to
break down proteins.
Skin, hair, and nail problems are not the only effects of biotin
deficiency. It can also cause depression, lethargy, susceptibility to
infections, neurological disorders, and increased cholesterol levels in
the blood. However, let me issue a serious WARNING here: the list
of symptoms caused by any vitamin deficiency is formidable. Most
people reading them feel the symptoms apply to them in some way.
But it is important to remember that you can catch a cold or feel a bit
lethargic without jumping to the conclusion that you have a biotin
deficiency. And cholesterol levels are more likely to be raised by
eating a big plate of bacon for breakfast than by eating the avidin in
an undercooked egg.
However, some people in higher-risk groups may well consider
the possibility of a biotin deficiency. That includes anyone who takes
antibiotics for an extended period, heavy drinkers, anyone who has
had part of their small intestine removed, anyone reliant on dialysis,
and people on certain kinds of medication. These people require
more biotin than they can get from a normal diet. One healthy
higher-risk group is pregnant women: developing babies use up
biotin like aging refrigerators gobble up electricity.
So far, no scientific studies have been carried out to investigate
how much biotin our gut bacteria provide us with. We know that they
produce some, and that antibacterial medications such as antibiotics
can cause biotin deficiency. Investigating whether members of the
Prevotella enterotype are more likely to suffer from a biotin
deficiency than someone of the Bacteroides enterotype would be a
pretty exciting research project. But, since the existence of the three
different enterotypes was only discovered in 2011, there are many
more pressing questions we need to answer.
It is not only their good output that makes Bacteroides so
successful; they also work hand in hand with others. Some species
in the gut make a living by clearing away the waste left by
Bacteroides. This is a win-win situation: Bacteroides work better in
tidy surroundings, and the waste-disposal organisms have a secure
source of income. On a different level, we find the composters.
These organisms not only utilize waste products for their own ends,
they also use them to make products that Bacteroides can use in
turn. For some metabolic pathways, Bacteroides themselves take on
the role of composter. For example, if they need a carbon atom to
modify a molecule, they simply reach up and grab it out of the
atmosphere in the gut. They always find what they are looking for,
since carbon is a waste product of our metabolism.
Prevotella
the Prevotella family is the opposite of Bacteroides.
Studies have shown that they are more common in the guts of
vegetarians, but they also appear in moderate meat eaters and in
convinced carnivores. Our diet is not the only factor that influences
the colonization of our gut. But more about that presently.
Prevotella also have a group of bacterial colleagues they prefer
working with—Desulfovibrionales. Desulfovibrionales often have a
long flagellum—a whiplike tail used to propel them along—and so,
like Prevotella, they are adept at trawling through our mucus
IN MANY WAYS,
membranes looking for useful proteins. They then either eat those
proteins or use them to build who-knows-what. Prevotella produce
sulfur compounds when they work. The smell of these compounds is
familiar, as we know it from boiled eggs. If it weren’t for
Desulfovibrionales whipping around with their propeller-tails,
snapping up the sulfur, Prevotella would soon find themselves
drowning in a sulfur swamp of their own making. Incidentally, this gas
is not dangerous to human health. Our nose wrinkles at it as a
precautionary measure as it can slowly become toxic as
concentrations increase a thousandfold.
Another substance that contains sulfur and has an interesting
smell is the vitamin associated with this enterotype: thiamine. Also
known as vitamin B1, this is one of the most widely recognized and
important vitamins. Our brains require it not only to keep the nerves
well nourished, but also to coat them in an electrically insulating
layer of fat. This explains why a thiamine deficiency may be the
cause of muscle tremors and forgetfulness.
A very serious lack of vitamin B1 causes a disease called
beriberi. It was described in Asia as early as AD 500. Beriberi means
“I cannot, I cannot” in the Sinhalese language of Sri Lanka and refers
to the fact that sufferers have difficulty walking due to nerve damage
and muscle atrophy. It is now known that polishing rice removes the
vitamin B1 it contains, and a diet made up predominantly of this kind
of rice leads to an onset of symptoms within a few weeks.
While not resulting in serious neurological or memory disorders, a
less severe vitamin B1 deficiency can cause irritability, frequent
headaches, and lack of concentration. More advanced cases can
cause a susceptibility to edema and heart problems. But once again,
beware: these symptoms can have many causes. They are only a
reason for concern when they are unusually frequent or severe.
They are rarely caused exclusively by a vitamin deficiency.
Studying the symptoms of vitamin deficiencies provides a useful
insight into the part played by vitamins in certain processes. Anyone
whose diet does not consist exclusively of polished white rice or
alcohol is usually well supplied. The fact that our gut bacteria help
supply us with essential vitamins means they are far more than just a
load of flagellating sulfur-poopers—and that is what makes them so
fascinating.
Ruminococcus
on this family—scientific opinions, at any rate.
Some scientists who decided to investigate the existence of
enterotypes for themselves found Prevotella and Bacteroides, but no
Ruminococcus group. Others swear this third group exists, and yet
others insist there is even a fourth or fifth group, or more. Such a
state of affairs can really ruin the coffee break at a medical congress.
Let’s agree for the sake of argument that there is at least a
possibility that this group exists. Its proposed favorite food is the cell
walls of plants. Possible colleagues include Akkermansia bacteria,
which break down the mucins in mucus and absorb sugar pretty
quickly. Ruminococcus produces a substance called haem, which
the body needs for many things, including producing blood.
One character who probably had problems producing haem was
Count Dracula. A genetic defect has been identified in his home
country, Romania, that results in symptoms that include a lack of
tolerance to garlic, sensitivity to sunlight, and the production of red
urine. This urine discoloration is caused by a defect in blood
production that means sufferers excrete the unfinished precursors of
blood production. Nowadays, those affected by the condition—called
porphyria—are given medical treatment rather than the starring role
in a horror story.
OPINIONS ARE DIVIDED
Even if the Ruminococcus enterotype does not exist, there is no
doubt that these bacteria are present in our gut. So, it is useful that
we now know more about them—and about Dracula and red pee.
Our bacteria-free laboratory mice have trouble forming haem, and so
it stands to reason that bacteria are somehow important in this
process.
Now we are more familiar with the tiny world of the microbes in
our gut. Their genes represent a huge pool of borrowed abilities.
They help us digest our food, and they produce vitamins and other
useful substances. We are just beginning to recognize enterotype
commonalities and search for patterns. And we do this for one
reason: 100 trillion tiny creatures reside in our gut and that cannot
but have an effect on us. So, let’s now go one step further and
explore the palpable effects they have on us. Let’s take a closer look
at how these gut bacteria affect our metabolism, and examine which
ones do us good and which ones do us harm.
The Role of the Gut Flora
SOMETIMES WE TELL fibs to our children. We do it because these little
untruths are so nice. There’s the one about the man with the big
white beard who arrives once a year on his tuned-up reindeer sleigh
piled high with children’s presents, or the one about the Easter
bunny hiding chocolate eggs in the garden. Sometimes, we don’t
even realize when we are not telling the truth—like when we
encourage a toddler to eat up: “One spoon for Daddy, one spoon for
Mummy, one for Granny, and one for Granddad . . .” If we wanted to
encourage Junior in a scientifically correct way, we would have to
say, “One spoon for you, baby. A small part of the next spoon for
your Bacteroides bacteria. An equally small part for your Prevotella.
And a teeny-weeny bit for a few other microorganisms waiting in
your tummy to be fed.” We might well send a friendly vote of thanks
down to the micro-colleagues enjoying the meal in baby’s belly. After
all, Bacteroides and company work hard to help keep baby well fed.
And not only in infancy. Adults, too, receive nutrition back from their
bacterial gut-dwellers, morsel by morsel. Gut bacteria process food
that we cannot break down unaided and share the results with us.
The idea that the bacteria in our gut might influence our overall
metabolism, and therefore our weight, is only a couple of years old.
The basic concept is that bacteria do not steal anything from us
when they share our food in this way. Very few gut bacteria reside in
the small intestine, where we break down our food for ourselves and
absorb the nutrients from it. The highest concentration of bacteria is
found where the digestive process is almost finished and all that
remains is for the undigested remnants to be transported away. The
farther you travel from the small intestine toward the final exit from
the gut, the more bacteria you will find per square inch of gut
membrane. It is our gut that makes sure this remains so. If the
equilibrium is disturbed and large numbers of overconfident bacteria
migrate to the small intestine, we have a case of what doctors call
bacterial overgrowth. This relatively unexplored condition causes
symptoms that can include severe bloating, abdominal pain, joint
pain, and gastrointestinal infections, as well as nutrient deficiencies
and anemia.
In ruminants such as cows, this construction design is reversed.
These large animals pride themselves on their ability to survive by
eating only grass and a few other plants. No other animal on the
farm would make fun of them for being puny vegans, so what is their
secret? Cows keep their bacteria right at the top of their digestive
tract. They don’t even bother trying to digest their food themselves
first, but pass the complex plant carbohydrates straight on to
Bacteroides and company. Their microbes turn these carbohydrates
into an easily digested feast for the cow.
It can be practical to keep your bacteria so close to the beginning
of your digestive tract. Bacteria are rich in protein—so, from a food
point of view, they are tiny little steaks. When they have finished their
life’s work in the cow’s stomach, they slip farther down the system,
where they are digested. They are a large source of protein for the
cow—tiny microbial tenderloins, bred by themselves. Our bacteria
are too far down the system to provide this practical steakhouse
service so we pass them out of our gut undigested.
Rodents keep their microbes as far down the system as we do,
but are more loath to waste the bacterial protein they contain. Their
simple solution is to eat their own feces. We don’t do that, preferring
to buy meat or tofu at the supermarket to compensate for the fact
that we are unable to process protein-rich bacteria in our large
intestine. However, we still benefit from the work of our bacteria,
even if we don’t digest them. Bacteria produce nutrients that are so
tiny we can absorb them directly into the cells of our gut.
Bacteria can also perform this service outside the gut. Yogurt is
nothing other than milk that has been predigested by bacteria. Much
of the sugar in the milk (lactose) has already been broken down and
transformed into lactic acid (lactate) and smaller sugar molecules.
That is why yogurt is both sweeter and sourer than milk. The newly
formed acid has another effect on the milk. It causes the milk protein
to curdle, giving the yogurt its characteristic thick consistency.
Predigested milk (yogurt) saves our body some work—we just have
to finish off what the bacteria started.
It is an especially good idea to employ those bacteria to predigest
our food that manufacture healthy end products. Mindful yogurt
manufacturers often use bacteria that produce more dextrorotatory
(right-turning) than levorotatory (left-turning) lactic acids. Molecules
of the two kinds of lactic acid are mirror images of each other.
Feeding the human digestive system with levorotatory lactic acid
molecules is like giving a left-handed pair of scissors to a righthanded person: they’re hard to handle. That is why it is a good idea
to pick yogurt from the supermarket shelves that states on the
container: “Contains mainly dextrorotatory [or right-turning] lactic
acid.”
Bacteria do more than just break down our food. They also
produce completely new substances. Fresh cabbage, for example, is
less rich in vitamins than the sauerkraut it can be turned into—those
extra vitamins are made by bacteria. Bacteria and fungi are
responsible for the taste, creamy consistency of, and holes in
cheese. Bologna sausage and salami are often made with starter
cultures—that’s butchers’ code for “We daren’t tell it you straight, but
it is the bacteria (mainly Staphylococcus) that make it so tasty.”
Lovers of wine or vodka appreciate the metabolic end product of
yeasts—known as alcohol. The work of these microorganisms does
not end in the wine barrel. Almost none of what a wine taster will tell
you is actually to be found in the bottle. The wine’s bouquet, for
example, develops so late because bacteria need time to do their
work. They sit in waiting at the back of the tongue, where the
process of transforming what we eat or drink begins. The substances
they release during that process create the aftertaste so appreciated
by the wine lover. And each connoisseur will experience a slightly
different taste depending on the population of bacteria on their
tongue. Still, it’s nice to get such an enthusiastic reaction to the
presence of these much-maligned microbes.
The bacteria population of our mouth is only about one-tenthousandth of the number that live in the gut, yet we still taste the
results of their work. Our digestive tract should be grateful for the
fact that it has such a large population with such a wide range of
skills. While simple glucose and fructose are easily digested, many
people’s guts start to flag when it comes to lactose, the sugar
contained in milk. Their owners then suffer from a lactose
intolerance. Complex plant carbohydrates would flummox a gut if it
were expected to have at the ready every enzyme needed to break
them down. Our microbes are experts in dealing with these
substances. We provide them with somewhere to live and the
undigested remains of our food—and they keep busy dealing with
the stuff that’s too complicated for us to do.
In the industrialized world, about 90 percent of our nutrition
comes from what we eat, and we are fed about 10 percent by our
bacteria. So, after nine lunches, meal number ten is on the house, so
to speak. Feeding adults is the main occupation of some of our
bacteria. That does not mean that it makes no difference what we
eat—far from it. And the kind of bacteria that are feeding us also
makes a big difference. In other words, if we are concerned about
our weight, we need to think about more than just the big, fat calories
we consume and remember that our bacteria are at the dinner table
with us.
How Might Bacteria Make
Us Fat?
Three Theories
1. “Chubby” Bacteria
might include too many bacteria that program a person
for chubbiness. These chubbiness-inducing bacteria are efficient at
breaking down carbohydrates. If the number of chubby bacteria gets
out of hand, we have a problem. Skinny mice excrete a certain
quantity of indigestible calories while their overweight peers excrete
significantly fewer. The chubby bacteria in the latter group extract
every last smidgen of energy from the same amount of food and
cheerfully feed it to Mr. or Ms. Mouse. For humans, that can mean
some people pile on the pounds even though they eat no more than
others. It could be that their gut flora is extracting more energy from
the food they eat.
How can that be possible? Bacteria are able to make various
fatty acids out of indigestible carbohydrates. Vegetable-loving
bacteria tend to manufacture fatty acids for the gut and the liver, and
THE GUT FLORA
others produce fatty acids that feed the rest of the body. A banana is
less likely to make you fat than half a chocolate bar containing the
same number of calories. That is because plant carbohydrates are
more likely to attract the attention of bacteria that provide fatty acids
to local customers like the liver. The chocolate bar, on the other
hand, is more likely to attract the attention of the full-body feeders.
Studies carried out on obese subjects show that they have less
overall diversity in their gut flora and that certain groups of bacteria
prevail—primarily those that metabolize carbohydrates. To succeed
in becoming obese, however, a few other conditions must be met.
Experiments with laboratory mice showed that some weighed 60
percent more at the end of the trial than at the beginning. Full-bodyfeeding bacteria cannot cause so much weight gain alone. This
prompted scientists to consider another marker for extreme weight
gain: inflammation.
2. Inflammation
metabolic problems, such as obesity, diabetes,
and high blood-lipid levels, usually have slightly increased levels of
infection markers in their blood, too. These infections are not so high
that they require treatment, as they would, say, if they were caused
by an infected wound or septicemia. That’s why doctors call these
subclinical infections. If there is anyone who knows a thing or two
about infection, it’s bacteria. They have a signaling substance on
their surface that tells the body when to get infected.
When we get injured, this reaction is useful. Infection reactions
flush out bacteria or attack them. As long as bacteria remain in their
cozy mucus-membrane home in the gut, this signaling substance
goes unnoticed. But when bacteria appear in disadvantageous
combinations, or when their host eats an overly fatty diet, too many
PATIENTS WHO HAVE
of them can find their way into the bloodstream. The body then slips
into low-key infection mode. From the evolutionary point of view, it’s
worth paying that price to build up fat reserves for leaner times.
Bacterial-signaling substances can also latch onto other organs
and affect metabolism from there. In rodents and humans, they dock
onto the liver or the fatty tissue itself and encourage the deposition of
more fat. They also have an interesting effect on the thyroid gland.
Bacterial infections hinder its function, causing it to produce fewer
thyroid hormones, slowing the rate at which the body burns fat.
Unlike acute infections, which cause weight loss or even
emaciation, subclinical infection causes weight gain. Bacteria are not
the only possible cause of subclinical infections—hormone
imbalances, too much estrogen, lack of vitamin D, or too much
gluten-rich food have all been observed to have a similar effect.
3. Cravings
for a crazy idea! A hypothesis postulated in
2013 suggests that gut bacteria can affect their host’s appetite.
Roughly speaking, the theory is that late-night cravings for
chocolate-covered toffees followed by an entire bag of party pretzels
do not originate in the organ that calculates our tax returns. Not our
brains but our guts are the home of gangs of bacteria that crave
hamburgers after three days on a diet. Somehow they manage to
pass on that message in a very persuasive way, because we find it
almost impossible to deny them any wish.
To understand this hypothesis, we have to try to get our head
around the issue of food. Faced with the choice between two
different dishes, we make the decision based on what we happen to
fancy at that moment. The amount of our chosen dish that we
actually eat is controlled by the feeling of satiety. In theory, bacteria
NOW, BRACE YOURSELF
have ways and means of influencing both those things. Again, we
can currently only conjecture that they also have a say in our
appetite. But in evolutionary terms, it is not such a silly idea. What
and how much we eat can be a matter of life and death for them. In
three million years of coevolution, even simple bacteria have had
time to adapt optimally to life with their human hosts.
If you want to trigger a craving for specific foods, you have to
gain access to the brain. That is no mean feat. The brain is wrapped
in a sturdy membrane called the meninges. Even more impenetrable
than the meninges are the coats that surround all the blood vessels
passing through the brain. The only things that can make it through
this tangled mess are pure sugar, minerals, and anything that is as
small and fat-soluble as a neural transmitter. Nicotine, for example,
makes it through to the brain, where it triggers reward signals or a
feeling of relaxed alertness.
Bacteria can produce particles that are small enough to make it
through the coating of the blood vessels into the brain. Examples
include tyrosine and tryptophan. These two amino acids are
converted into dopamine and serotonin in the cells of the brain.
Dopamine? Wasn’t that famously associated with the brain’s reward
system? And serotonin? That sounds familiar, too, doesn’t it? Lack of
it causes depression. It can make us feel contented and sleepy. Just
think about last year’s Christmas dinner. Did you end up dozing on
the couch after enjoying it, feeling lethargic and sleepy but also
contented?
So the theory is this: our bacteria reward us when we send them
a decent delivery of food. It feels pleasant and whets our appetite for
the next meal. They do this not only directly by means of the
substances they produce, but also by cranking up the body’s
production of certain transmitters. The same principle applies to the
feeling of satiety.
Several studies have shown our satiety signal transmitters
increase considerably when we eat the food our bacteria prefer.
What our bacteria prefer is food that reaches the large intestine
undigested, where they can then gobble it up. Surprisingly enough,
those foods do not include pasta and white bread ;-). For more on
this, turn to the section on prebiotics in the last chapter of this book.
The feeling of satiety generally comes from two sides: from the
brain and from the rest of the body. A lot can go wrong here. In
obese people, the gene that codes for satiety can be defective, and
such people simply do not get that full feeling after eating. According
to the selfish brain theory, the brain does not receive enough of the
energy eaten as food and so decides that it is still hungry. But it is
not only our body tissue and our gray matter that depend on the food
we eat—our microbes also need to be fed. They may seem small
and insignificant by comparison with our body size—accounting for
just 4½ pounds (2 kilos) of our body weight. So what right do they
have to butt in?
When we consider the range of functions carried out by our gut
flora, it is not surprising that these microbes are also able to express
their wishes. They are, after all, the immune system’s most important
trainers, digestion assistants, producers of vitamins, and experts in
detoxifying moldy bread or medical drugs. The list is actually much
longer, of course, but the message should be clear: they should be
able to have a say in whether we feel full after eating.
We do not yet know whether different bacteria express different
desires. When we give up sweets, we eventually stop missing them
so badly at some point. Is that because the gummy bear and
chocolate lobby has been starved out? We can only speculate.
The important thing is not to reduce the human body to a twodimensional cause-and-effect machine. The brain, the rest of the
body, bacteria, and the elements in our food all interact with each
other in four dimensions. Striving to understand all these axes is
surely the best way to improve our knowledge. However, we can
more easily tinker with bacteria than with our brain or our genes—
and that is what makes microbes so fascinating. The nutrition we
receive from our bacteria is not only important for fighting the flab, it
also affects the levels of fats such as cholesterol in our blood. This
realization could be quite highly charged as obesity and high
cholesterol levels are closely connected with the greatest health
issues of our time: hypertension, arteriosclerosis, and diabetes.
Cholesterol and Gut Bacteria
bacteria and cholesterol was first
discovered in the 1970s. American scientists studying Maasai
warriors in Africa had been surprised to find the levels of cholesterol
in their blood were low, despite a diet consisting almost entirely of
meat and milk. This excessive amount of animal fat did not cause
high blood-lipid levels. The scientists suspected a mysterious
substance in the milk they drank might be causing their cholesterol
levels to remain low.
The scientists then set about doing all they could to find that
mysterious ingredient. They tested cow’s milk and camel’s milk and
even rat’s milk. Sometimes they managed to reduce cholesterol
levels, sometimes not. These results told the scientists nothing. In
another experiment, they gave the Maasai warriors a vegetablebased milk replacement product (Coffee-mate®) with high levels of
cholesterol added to it. Still, the subjects’ blood cholesterol levels did
not rise. The scientists saw that their theory about a mysterious milk
component was disproven.
They had meticulously noted that the Maasai often drank curdled
milk, but no one considered the fact that certain bacteria are required
THE CONNECTION BETWEEN
to curdle milk. That would have explained the results of their Coffeemate® experiment. Bacteria that have already settled in the gut can
continue to live there even when milk is replaced with plant-based
creamer enriched with cholesterol. Even when the Maasai’s
cholesterol levels were seen to sink by 18 percent whenever they
drank curdled milk rather than fresh milk, scientists continued to
search for the mysterious milk substance—blind dedication that
brought no results.
These studies of the Maasai would not live up to modern
scientific expectations. The test groups were too small, and the
Maasai spend about thirteen hours a day walking and one month a
year fasting. They simply cannot be compared to meat-eating
Westerners. However, the results of these studies were rediscovered
decades later by researchers who were now aware of the
importance of bacteria. Cholesterol-lowering bacteria? Why not test
that in the lab? Take a flask of nutrient broth warmed to a balmy 98.6
degrees Fahrenheit (37 degrees Celsius), add cholesterol and some
bacteria—et voilà! The bacterium they used was Lactobacillus
fermentus, and the cholesterol they had added was . . . gone! At
least a considerable proportion of it was.
Experiments can have very different results, depending whether
they are carried out in glass flasks or inside opisthokonts. It’s like an
emotional rollercoaster ride for me when I read in scientific papers
sentences like “The bacterium L. plantarum Lp91 can significantly
lower high cholesterol and other blood lipid levels, increase good
HDL cholesterol, and lead to significantly lower rates of
arteriosclerosis, as could be shown in 112 Syrian golden hamsters.” I
have never been so disappointed by Syrian golden hamsters.
Experiments on animals are a good way to begin tests on living
systems, but if the sentence had ended “as could be shown in 112
obese Americans,” the whole thing would be a lot more impressive.
But a result like that can still be worth a lot. Studies on mice, rats,
and pigs yielded such promising results for some bacteria that
scientists considered it reasonable to begin human testing. The
subjects were regularly administered certain bacteria and after a
period of time their cholesterol levels were measured. The bacteria
species, the quantities, the duration, and the way they were
administered were all varied. Some results were positive and others
were not. Also, no one really knew whether sufficient numbers of the
administered bacteria even survived their bath in the acid juices of
the stomach long enough to have an effect on blood cholesterol
levels.
Really valuable studies began about twenty years ago. For one
experiment in 2011, 114 Canadians ate specially produced yogurt
twice a day. The bacterium added to the yogurt was Lactobacillus
reuteri—in a form particularly resistant to digestion. Within six weeks,
their levels of bad LDL cholesterol sank by 8.91 percent. That’s
about half the improvement attained by taking a mild anti-cholesterol
drug—but without the side effects. Studies using other types of
bacteria lowered cholesterol levels by as much as 11 to 30 percent.
Follow-up research still needs to be carried out to verify these
promising indications.
There are several hundred bacteria candidates that might be
tested in future. To sift out the less likely ones, we have to ask the
following kinds of questions. What abilities does such a bacterium
need to have? Or rather, “What genes does it need to have?” The
most likely candidates we know of today are BSH genes. BSH
stands for bile salt hydrolase. Bacteria with these genes can convert
bile salts. But what do bile salts have to do with cholesterol? The
answer is in the name. Cholesterol comes from the Greek words
chole (bile) and stereos (solid). Cholesterol was first discovered in
gall stones. Bile, which is stored in the gall bladder, is the body’s
transport medium for fats and cholesterol. BSH allows bacteria to
alter bile to make it work less efficiently. The cholesterol and fat
dissolved in bile can then no longer be absorbed by the body and
they end up, to put it bluntly, down the toilet. This mechanism is
useful for bacteria because it weakens the effect of bile, which can
attack their cell membranes. This protects the bacteria on their long
journey to their final destination—the large intestine. Bacteria also
have a few other mechanisms for dealing with cholesterol: they can
absorb it directly and incorporate it in their cell walls, they can
convert it into a new substance, or they can manipulate organs that
produce cholesterol. Most cholesterol is produced in the liver and the
gut, where tiny messenger substances manufactured by the bacteria
can partly control those processes.
But we need to take a step back and ask cautiously: does the
body always want to get rid of its cholesterol? It produces between
75 and 90 percent of our cholesterol itself. And that takes a lot of
work! One-sided media reporting has given cholesterol a bad name,
making people believe it is only evil. That is quite wrong. Too much
cholesterol is not such a good thing, but neither is too little. If it
weren’t for cholesterol, we would have unstable cells and no sex
hormones or vitamin D. Fat and cholesterol are not only an issue for
Granny and her weakness for cream cakes or sausages. They are
an issue for every one of us. Studies have shown a connection
between too little cholesterol and memory problems, depression, and
aggressive behavior.
Cholesterol is also the miraculous base material for building all
sorts of structures. Too much of it is indeed harmful—it’s all about
finding the right balance. Our bacteria would not be our bacteria if
they didn’t have the ability to help us achieve that. Some bacteria
produce more of a substance called propionate, which inhibits the
production of cholesterol. Others produce more acetate, which
promotes the production of cholesterol.
Who would have thought it? A chapter that began with bright,
little spots of bacteria ending with concepts like appetite and satiety
or substances like cholesterol? To summarize: Bacteria help to feed
us, make some foods more digestible, and produce their own
substances. Some scientists now support the theory that our gut
microbiota can be considered an organ. Just like the other organs in
our body, this organ has an origin, develops along with us, is made
up of a load of cells, and is in constant contact with its fellow organs.
The Bad Guys—Harmful Bacteria and
Parasites
THERE ARE GOOD guys and there are bad guys in the world—and the
same goes for the world of our microbes. One thing unites most of
the bad guys: they only want what’s best . . . for themselves.
Salmonellae in Hats
courageous of cooks sometimes feel a pang of primal
fear while beating eggs—fear of the raw threat posed by Salmonella!
Everyone knows someone who has endured devastating diarrhea
and venomous vomiting after eating chicken that was not quite done
or nibbling on a bit of raw cake mix.
Salmonella bacteria can get into our food in unexpected ways.
Sometimes, globalization helps them find a home in our chicken,
meat, or eggs. This is how it can happen in Germany, where I live.
The cheapest source of feed grain for chickens is Africa. So, we fly it
in to feed the fowl in our poultry farms. However, there are more wild
tortoises and lizards wandering around in Africa than Germany.
Salmonella bacteria travel to our climes along with the chicken feed.
How so? Well, they are part of the normal gut flora of reptiles. While
the African farmer is working in the fields, a tortoise might merrily be
doing its business in a sack of grain destined for Germany. After an
EVEN THE MOST
exciting flight with a wonderful view over the clouds, the grain, along
with its stowaway tortoise-poop bacteria, ends up in a German
poultry farm, where it is eaten by a hungry chicken. Salmonella
bacteria are not part of a chicken’s natural gut flora, but they are a
common pathogen. Similar contamination can occur in other
countries when animal feed contains materials where Salmonellae
may lurk.
Once inside the bird’s gut, the Salmonellae can multiply, and they
are eventually excreted. Since chickens have only one hole for all
export goods, the egg cannot avoid coming into contact with
Salmonellae in the bird’s feces. The bacteria are then found only on
the shells of eggs—they only get inside when the shell is cracked.
But what about Salmonellae in chicken meat? How do they get
there? That’s a rather unsavory story. Cheaply fed chickens are
usually sent to large industrial slaughterhouses to meet their maker.
Once they have been slaughtered and beheaded, they are dunked in
huge tanks of water. Those tanks are like a wellness spa for
Salmonella bacteria, complete with a colonic irrigation service for the
chickens. In a slaughterhouse dispatching 200,000 birds a day, one
batch of cheap-feed chickens is enough to give the gift of Salmonella
to all the other birds in the bath. The chickens then end up in the
freezers of discount supermarkets. If they are roasted or grilled at
high-enough temperatures, the Salmonella germs are soon killed off
and can no longer cause problems for anyone.
Properly cooked meat is normally not the reason for most
Salmonella infections. The problems begin when the frozen chicken
is left to thaw in the kitchen sink or colander. Freezing and thawing
does bacteria little harm. The huge library of bacteria in our
laboratory includes germs, collected from patients, that easily survive
temperatures of minus 112 degrees Fahrenheit (minus 80 degrees
Celsius) and live merrily on when thawed. Heat is their nemesis.
Even just ten minutes’ exposure to a temperature of 167 degrees
Fahrenheit (75 degrees Celsius) is enough to see off all Salmonella
bacteria. That’s why a carefully roasted chicken is not usually the
culprit, but rather the lettuce leaves for the side salad, left to soak
briefly in the same kitchen sink.
We come into regular contact with the gut flora of the livestock we
keep, but we only notice it when they happen to include unfamiliar,
diarrhea-causing bacteria. The rest is routine, so to speak, and after
all, we have to get our bacteria from somewhere. Sticking to organic
country eggs from chickens fed with home-grown grain is usually a
reliable way to avoid dangerous bacteria—unless the farmer himself
eats cheap chicken from a discount supermarket.
If our Sunday roast chicken is not roasted enough, we can end
up eating not just chicken muscle cells but a few Salmonella cells,
too. It takes between ten thousand and one million of these singlecelled creatures to put us out of action. A million of these bacteria
take up about one-fifth as much space as a grain of salt. So, how
does an army of such tiny soldiers manage to move a colossus like
us—with the volume of about 600,000,000 grains of salt—inexorably
toward the toilet? It’s as if one hair of the American president’s head
were to rule over the entire population of the United States.
Salmonella bacteria double in number much more quickly than
politicians’ hairs—that’s point one. As soon as the temperature rises
above 50 degrees Fahrenheit (10 degrees Celsius), Salmonellae
come out of hibernation and get busy breeding. They have delicate
little arms that enable them to swim around until they find a place to
attach to the gut. Once there, they invade our cells, which become
infected and pump large quantities of fluid into the gut in an attempt
to flush out the pathogen as quickly as possible.
It can take a few hours to a few days from accidental ingestion to
watery flush-out. A self-induced colonic irrigation like this usually
works well, unless the victim is too young, too old, or too frail.
Antibiotics would do more harm than good here. Despite this natural
cure, it is better for the gut to flatly refuse entry to Salmonella,
however rude that may seem. After a visit to the toilet or a retching
session into a sick bag, you should not take them by the hand and
show them what life is like in the outside world. They should be given
the cold shoulder by washing with very hot water and soap to let
them know: it’s not you, it’s me—I just can’t deal with your clinging
personality.
Salmonellae are the most common type of bad guys we take in
with our food. They are not found exclusively in poultry products, but
poultry products are one of Salmonellae’s favorite hang-outs.
Salmonellae come in several varieties. When we receive stool
samples from patients at our laboratory, we can test them by
exposing them to different antibodies. When an antibody bonds with
the Salmonellae, they clump together into blobs that are big enough
to see with the naked eye.
When that happens, we can say that the antibody to vomitinducing Salmonella XY reacts strongly, so this must be vomitinducing Salmonella XY. This is the same as the mechanism in our
own body. Our immune system meets a couple of new Salmonellae
and says, “Hmmm, I’m sure I must have a hat that fits them
somewhere in my collection.” It then rummages around in its
wardrobes to find the right hat, adjusts it a little to create the perfect
fit, then commissions a hatter to make headgear for a million
Salmonella germs. When all the Salmonella bacteria are wearing
their new hats, they no longer look dangerous, but rather ridiculous.
They are weighed down so much by the millinery that they are too
heavy to swim around attacking anything. In this way, the test
antibodies in the lab can be seen as a small selection of different
hats. When the hat fits, the heavily sombreroed bacteria collapse
into clumps and—depending on the hat—we can say which type of
Salmonella was in the stool sample.
For those who do not necessarily want to send their immune
system searching for hats and who are no great fans of diarrhea and
vomiting, there are a few simple rules to follow.
Rule number one: Always use plastic chopping boards because
they are easier to clean properly and provide fewer grooves and
ridges for bacteria to hide in.
Rule number two: Always wash anything that comes into contact
with raw meat or eggshells thoroughly with hot water—chopping
boards, hands, cutlery, kitchen sponges, and colanders, for example.
Rule number three: Whenever possible make sure that meat and
egg-based foods are cooked through. Of course, that doesn’t mean
you have to interrupt your romantic dinner to stick the tiramisu in the
microwave. If you are planning a dish of that sort, make sure you
always use good-quality, fresh eggs and always store them at a
temperature of less than 50 degrees Fahrenheit (10 degrees
Celsius).
Rule number four: Think beyond the kitchen. Anyone who has
had to rush to the toilet after feeding their pet iguana and then
themselves (without washing their hands properly) will remember my
words: Salmonella bacteria are part of the normal gut flora of
reptiles.
Helicobacter pylori—Humanity’s First Pet
HEYERDAHL WAS a phlegmatic man with strongly held views.
He observed ocean currents and winds. He was interested in ancient
fishhooks and clothing made of tree bark. All this convinced him that
the Polynesian islands were first colonized by seafarers from South
America and Southeast Asia. He theorized that they could have used
currents to help them reach the islands on rafts. At the time, no one
thought it possible that a simple raft could survive a five-thousandmile journey (eight thousand kilometers) across the Pacific.
Heyerdahl was not a man to waste time trying to convince doubters
with theoretical arguments. He went to South America, built a
primitive raft out of balsawood logs, grabbed a couple of coconuts
and cans of pineapple, and set out for Polynesia. After four months,
he could safely say, “Yes, it is possible!”
Thirty years later, another scientist set off on an equally exciting
expedition. But his journey did not take him across oceans; it took
him to a small laboratory with neon strip lighting on the ceiling.
There, Barry Marshall picked up a petri dish of liquid, placed it to his
THOR
lips, and bravely swallowed its contents. His colleague observed him
with interest as he did so. After a few days, Barry Marshall
developed a stomach inflammation and could proudly say, “Yes, it is
possible!”
Another thirty years went by before scientists in Berlin and
Ireland made a connection between the research of these two very
different pioneers. Marshall’s stomach bug was destined to provide
information about the first colonization of Polynesia. This time no one
sailed an ocean and no one drank a lab culture. Researchers asked
a few desert-dwelling Aboriginals in Australia and highland tribesmen
from New Guinea for a sample of their stomach contents.
It is a story about disproving prevailing paradigms, dedication to
research, a tiny creature with a propeller, and a big, hungry cat.
The bacterium Helicobacter pylori lives in the stomachs of at
least half of humankind. This insight is relatively new and was initially
ridiculed. Why should an organism live in such an inhospitable
environment? A cave full of acid and enzymes bent on breaking it
down? It takes more than that to discourage Helicobacter pylori. This
bacterium has developed two strategies that enable it to cope
excellently with that harsh environment.
Firstly, the products of its metabolism are so alkaline that they
can neutralize any acid in its immediate vicinity. Secondly, it burrows
beneath the mucus membrane that protects the stomach from
digesting itself with its acidic juices. This membrane usually has a
gelatinous consistency, but H. pylori is able to liquefy it so that it can
swim more easily through the mucoid lining. It has long threads of
proteins it uses as flagella to whizz around.
Marshall and Warren believed H. pylori caused stomach
inflammations (gastritis) and gastric ulcers. The prevailing scientific
opinion at the time was that those stomach problems were
psychosomatic in origin (as a result of stress, for example) or caused
when the stomach secreted too much acid. Marshall and Warren had
to both counter the preconception that nothing could survive in the
acid environment of the stomach and prove that a tiny bacterium
could cause diseases that were not traditional bacterial infections.
Until that time, it was believed that bacteria could only infect wounds,
and cause fevers and colds.
After the otherwise healthy Marshall deliberately swallowed H.
pylori bacteria and gave himself gastritis, which cleared up after a
course of antibiotics, it took another ten years before the scientific
world accepted his discovery. Today, it is standard practice to test
patients with stomach complaints for the presence of these bacteria.
The patient is given a fluid to drink and if H. pylori bacteria are
present in the stomach, they break down the ingredients of the fluid
and a marked, odorless gas can be identified in the breath of the
patient using a special machine. Drink, wait, breathe. A relatively
simple test.
What the two scientists did not realize is that they had not only
discovered a cause of illness, they had also discovered one of
humankind’s oldest pets. H. pylori bacteria have been living inside
human beings for more than fifty thousand years, and they have
evolved in tandem with us. When our ancestors began to migrate
around the world, H. pylori went along for the ride and founded new
populations, just like those human pioneers. Today, three African,
two Asian, and one European type of this bacterium have been
identified. The farther the population groups spread from each other
in both space and time, the greater the difference between their
stomach bacteria.
The slave trade transported the African types to America. In
northern India, the Buddhist and Muslim populations have different
strains in their stomachs. Families in industrialized nations often
have their own family strain of H. pylori, while people living in
societies with more contact between individuals, for example, in
parts of Africa, have communal H. pylori strains.
One out of four North Americans is a carrier for H. pylori. Not
everyone who carries it in their stomach is doomed to develop
stomach problems, but most people who do have stomach problems
have H. pylori to thank for their woes. This is because some H. pylori
bacteria are more dangerous than others. Two factors are known to
be responsible for the more virulent version. One is called CagA.
CagA enables the bacteria to inject certain substances into our cells
like a tiny syringe. The second factor is called VacA. VacA needles
the cells of the stomach continuously, causing them damage that is
eventually fatal to the cell. There is a much higher probability of
developing stomach problems if the H. pylori microbes in the
stomach possess the injecting-syringe or cell-damaging gene. If
those genes are not present, H. pylori is much less harmful as it
swims around in the stomach.
Although they share many similarities, each H. pylori bacterium is
as unique as the person carrying it. These bacteria adapt to their
host and change as she changes. Scientists can make use of this
fact to trace who infected whom with the germ. Big cats have their
own feline Helicobacter. Its name is Helicobacter acinonychis. The
fact that it bears such a resemblance to human Helicobacter raises
the question: who was eating whom in prehistoric times? Was it a
case of man eating tiger or tiger eating man?
Genetic analysis shows that the genes that were deactivated in
the feline version of the bacterium were mainly those that would
otherwise enable it to latch on to the cells of the human stomach—
but the reverse was not the case. When devouring a prehistoric
person, a large cat must also have devoured that person’s stomach
bacteria. These bacteria are not killed by even the sharpest of tiger
teeth, so Helicobacter colonized the stomach of the predator and its
descendants. A tiny bit of redress, at least.
But is H. pylori good or bad?
H. pylori Is Bad
stomach’s mucus membrane and swimming
around in it, H. pylori weakens this protective barrier. As a result, the
aggressive acids in our stomach digest not only our food, but a little
bit of our own stomach, as well. If the bacteria also possess the
injection-syringe or cell-damaging gene, our stomach cells have little
hope. About one-fifth of people who harbor this bacterium develop
tiny lesions in their stomach wall. Two-thirds of stomach ulcers and
almost all ulcers in the small intestine are caused by an H. pylori
infection. If the microbes can be wiped out with antibiotics, the
patient’s stomach problems disappear. A new product could soon
provide an alternative to antibiotics: sulforaphane, which is contained
in broccoli and similar vegetables. This substance is able to block
the enzyme that H. pylori uses to neutralize gastric acid. Those who
would like to try it as an alternative to antibiotics should make sure
they use very high-quality broccoli and consult their doctor after two
weeks to test whether their H. pylori population has really
disappeared.
Constant irritation is never a good thing. We are all familiar with
itchy insect bites. At some point we can no longer resist scratching
them to make the itching stop, even though we know we will end up
with a bleeding wound. Something similar happens with the cells of
the stomach. A chronic inflammation means the cells are
permanently irritated until they finally give up the ghost and break
down. In older people, this can also be a cause of appetite loss.
The stomach has a battery of stem cells, which constantly
replace lost cells. If these replacement manufacturers are
overworked, they may begin to make mistakes. Cancer cells are the
result. Statistically, this does not look too serious: around 1 percent
of H. pylori carriers develop stomach cancer. But if you bear in mind
that half of humanity harbor these bacteria in their stomach, 1
BY INFILTRATING OUR
percent turns out to be a pretty big number. The probability of
developing stomach cancer without the presence of H. pylori is about
forty times less than with it.
In 2005, Marshall and Warren received a Nobel Prize for their
discovery of the connection between Helicobacter pylori and
gastritis, stomach ulcers, and cancer. The journey from bacteria
cocktail in Perth to celebratory cocktail in Stockholm took twenty
years.
It took even longer for the connection between Helicobacter pylori
and Parkinson’s disease to be realized. Although doctors had known
since the 1960s that patients with Parkinson’s have an increased
incidence of stomach problems, they did not know the nature of the
connection between sore stomachs and trembling hands. It took a
study of different population groups on the Pacific island of Guam to
shed light on the subject.
In some parts of the island, there was an astonishingly high
incidence of Parkinson’s-like symptoms among the population.
Those affected suffered from trembling hands, facial paralysis, and
motor problems. Researchers realized that the symptoms were most
common in areas where people’s diets included cycad seeds. These
seeds contain neurotoxins—substances that damage the nerves. H.
pylori can produce an almost identical substance. When laboratory
mice were fed with an extract of the bacteria, without being infected
with the living bacterium itself, they displayed symptoms very similar
to those of the cycad-eating Guamanians. Once again, not every H.
pylori bacterium produces this substance, but for those people who
harbor the ones that do, it is not good news.
In summary, it can be said that H. pylori can manipulate our
protective barriers, irritate and destroy our cells, and manufacture
toxins and damage our entire body by doing so. So, how has our
vulnerable body been able to survive many millennia of infection with
this bad bacterium? Why have these bacteria been so widely
tolerated by our immune system for so long?
H. pylori Is Good
of H. pylori and its effects reached the following
conclusion. The bacterium, especially that much-feared strain with
the injection-syringe gene, can also interact with the body in
beneficial ways. After more than twelve years of observing over ten
thousand subjects, it was concluded that carriers of this type of H.
pylori do have an increased risk of stomach cancer, but their risk of
dying of lung cancer or a stroke was much lower. In fact, it was only
half that of other subjects in the study.
Even before this study, scientists had already suspected that a
bacterium that has been tolerated for so long cannot be only bad.
They had shown in experiments with mice that the H. pylori
bacterium provides a reliable protection against childhood asthma.
When the mice were given antibiotics, this protection disappeared
and the infant rodents stood a chance of developing asthma again.
When the bacterium was given to adult mice, the protective effect
was still present but much less pronounced. You might say mice are
not people, but this observation fits very well with the general trend
noticed in industrialized countries in particular. Rates of asthma,
allergies, diabetes, and neurodermatitis have risen as rates of H.
pylori have fallen. This observation is far from constituting proof that
H. pylori is the sole protection against asthma, but it may be part of
the overall picture.
The theory suggested to explain this correlation is that this
bacterium teaches our immune system to stay cool. H. pylori latches
onto our stomach cells and by doing so causes large numbers of
regulatory T-cells to be produced. Regulatory T-cells are immune
A LARGE-SCALE STUDY
cells whose job is to place a calming hand on the shoulder of the
immune system when it flies off the handle like a drunk in a crowded
nightclub. The T-cells say to the immune system, “Let us deal with
this, mate.” As the name implies, these cells regulate the immune
system’s reactions.
While the irate immune system is still shouting, “Get out of my
lungs you bloody pollen-thing!” and showing its readiness to fight by
giving us swollen, red eyes and a runny nose, the regulatory T-cells
say, “Oh come on, immune system, that was a bit of an overreaction.
The pollen-thing is only looking for a flower to pollinate. It’s just
landed here by mistake. That’s more of a problem for the pollen grain
than for us. It will never find its flower now.” The more of these
sensible cells there are at work, the more chill the immune system
will be.
When H. pylori causes a particularly large number of these cells
to be produced by one mouse, another mouse’s asthma can be
improved simply by transplanting those cells to it. That must be an
easier solution than training a mouse to use a tiny little inhaler!
The incidence of eczema seems to be reduced by about onethird in people who harbor H. pylori. Increases in inflammatory gut
disease, autoimmune problems, and chronic inflammations may also
be a modern trend caused by the fact that we often unwittingly wipe
out something that has protected us for millennia.
H. pylori Is Good and Bad
H. pylori ARE bacteria with many capabilities. They can’t be labeled
simply good or bad. It always depends on what exactly the bacterium
does inside us. Is it manufacturing dangerous toxins, or is it
interacting with our body to protect it in some way? Are our cells
constantly irritated, or can we produce enough gastric mucus for
both its needs and our own? What part is played by agents that
irritate the stomach’s mucus membrane, such as painkillers,
cigarette smoke, alcohol, coffee, and stress? Is it a combination of all
these that is responsible for stomach ulcers—because our little pets
don’t like them?
The World Health Organization recommends people with
stomach problems should get rid of the potential culprits. If stomach
cancer, certain lymphomas, or Parkinson’s disease run in the family,
it is also a good idea to offload H. pylori.
Thor Heyerdahl died in Italy in 2003 at the age of eighty-eight.
Had he lived just a couple of years longer, he would have seen his
theory about the colonization of Polynesia confirmed by studies of H.
pylori strains. Asian strains of H. pylori conquered the New World in
two waves, via the Southeast Asian route. But his theory about
South American origins has not yet been proven. Who knows what
bacteria still remain to be discovered before Heyerdahl’s theory is
confirmed by a microbiological voyage of discovery?
Toxoplasmata—Fearless Cat Riders
cuts her wrists with a razor blade from
the discount drugstore. It’s the thrill that makes her do it.
A fifteen-year-old racing-car fan crashes into a tree at full tilt. And
dies.
A rat drapes itself over the cat’s food dish in the kitchen,
presenting itself as a delicious meal.
What do these three have in common?
They are all failing to heed the internal signals that aim to
preserve the huge community of cells that makes up living creatures.
This community only wants the best for us. These three individuals
seem to be pursuing interests at odds with those of their body—
interests that may well have come out of a cat’s gut.
Cat’s guts are the home of Toxoplasma gondii. These tiny little
organisms consist of only one cell, but they are counted as animals.
They carry much more complex genetic information than bacteria.
Their cell walls are also constructed differently and they probably
lead more exciting lives.
Toxoplasmata reproduce in the guts of cats. The cat acts as their
definitive host and all the other animals that toxoplasmata use
temporarily as taxis to take them from cat to cat are defined as
intermediate hosts. A cat can get toxoplasmata only once in its life,
and the cat is a danger to people only during that time of infection.
Most older cats already have their toxoplasmata infection behind
them and so cannot harm us anymore. During a fresh infection,
toxoplasmata are found in the animal’s feces. They mature in the cat
A THIRTY-TWO-YEAR-OLD WOMAN
litter for about two days before they are ready to infect their next
host. If no cat happens to pass by but a dutiful, cat-owning mammal
comes and cleans the litter, these tiny protozoa seize the opportunity.
The microscopic creatures in the cat’s feces can wait up to five years
to infect another definitive host. Their intermediate host does not
necessarily have to be a human cat-lover. Cats and other animals
roam through gardens and vegetable patches and sometimes get
killed. One of the main vectors of toxoplasma infection is raw food.
The probability, in percent, of your having toxoplasmata yourself is
about as high as your age in years. On a global scale, about onethird of humans harbor them.
Toxoplasma gondii are counted as parasites because they cannot
live on just any little patch of earth and absorb water and plant tissue
—they need a little patch of organism to live on. As humans, we call
such creatures parasites because we get nothing in return. At least,
nothing positive, like monthly rent or affection. Quite the opposite, in
fact—some can harm us by means of a kind of human pollution.
They do not have any overly negative effects on healthy adult
hosts. Some people have mild, flu-like symptoms, but most notice
nothing. After the acute infection phase, the toxoplasmata move into
tiny apartments in our tissue and enter a kind of hibernation state.
They will never leave us for the rest of our lives, but they are quiet
little lodgers. Once we have been through this, we can never be
reinfected. We are already occupied, so to speak.
However, an infection like this can have drastic consequences for
pregnant women. The parasites can reach an unborn child via the
mother’s bloodstream. The immune system is not yet familiar with
them and is not fast enough to catch them. This does not necessarily
always happen, but when it does, it can cause serious damage and
even a miscarriage. If the infection is detected early enough, it can
be treated with medication. But the chances of that are slim, since
most people do not notice when they become infected. And in many
countries, for example, a toxoplasma scan is not part of the standard
set of pregnancy examinations. If your gynecologist starts asking
strange questions like “Do you own a cat?” at your initial pregnancy
examination, don’t brush the question off as meaningless small talk
—she’s clearly an expert in her field.
Toxoplasmata are the reason your cat’s litter should be changed
every day if there is a pregnant woman in the house (but not by
her!), why raw food should be avoided by mothers-to-be, and why
fruit and vegetables should always be washed. Toxoplasmata cannot
be transferred from person to person. Infection can only come from
the little residents of a freshly infected cat’s gut. But, as mentioned
earlier, they can survive for a long time, even on the hands of cat
owners. Once again, good old hand washing is the best defense.
So far, so good. All in all, toxoplasmata seem to be unpleasant
but otherwise unimportant little critters if you don’t happen to be
pregnant. And, for many years, no one paid them much attention—
but Joanne Webster’s fearless rats changed all that. In the 1990s,
Joanne Webster was a researcher at Oxford University. She devised
a simple but ingenious experiment. She placed four boxes in a small
enclosure. In one corner of each of these boxes, she placed a small
bowl containing a different liquid: rat urine, water, rabbit urine, and
cat urine. Even rats that have never seen a cat in their lives avoid cat
urine. They are biologically programmed to think, “If someone peed
there who might want to eat you, don’t go there.” Furthermore,
rodents have a general motto that goes something like this: “If
someone places you in an enclosure with boxes containing urine, be
on your guard.” Under normal circumstances, all rats behave the
same way. They briefly explore the unfamiliar environment and then
withdraw into one of the boxes with the less threatening urine in it.
But Webster found there were exceptions. There were rats that
suddenly displayed completely atypical behavior. They inquisitively
explored the whole enclosure, apparently oblivious to risk, even
defying their instincts and entering the box containing the bowl of cat
urine and hanging out there for a while. After observing them for
longer, Webster was even able to conclude that they seemed to
prefer the cat-urine box to the others. Nothing seemed to interest
them more than cat pee.
A smell that should have registered in their brain as sign of mortal
danger was suddenly perceived as attractive and interesting. These
animals had become uninhibited seekers of their own downfall.
Webster knew that there was only one difference between these rats
and normal specimens—they were infected with toxoplasmata. This
is an incredibly clever move on the part of the tiny parasites. They
cause the rats offer themselves as food to their definitive hosts!
This experiment caused such consternation in the scientific
community that it was repeated in other laboratories around the
world. Scientists wanted to make sure the results were not a fluke so
they tested to see whether their own lab rats would act in the same
way if they were infected with toxoplasmata. And they did. The
experiment is now considered flawless and scientifically sound.
Scientists also discovered that the change in behavior was related
only to the rats’ response to cat urine, while dog urine elicited the
expected avoidance behavior.
These results whipped up a storm of debate. How could such tiny
parasites influence the behavior of little mammals so drastically? To
die or not to die? That is a huge question that any organism worth its
salt should be able to answer—as long as there is no parasite on the
decision-making committee. Surely?
It was not much of a leap from the little mammal to a larger
mammal (that is to say, to human beings). Might it be possible to find
human candidates who succumb to a kind of “feed myself to the cat”
instinct in the form of inappropriate reflexes, reactions, and
fearlessness? One approach to finding an answer to this question
was to test the blood of people who had been involved in traffic
accidents. The quest was to find out whether more of the unfortunate
road users would turn out to be toxoplasma carriers than members
of society who had not been involved in an accident.
The answer was yes. The risk of being involved in a traffic
accident is higher among toxoplasma carriers, especially when the
infection is in the active early stage rather than the later dormant
stage. Three small initial studies were followed by a large-scale
investigation, and all of them confirmed these results. The largescale study involved taking blood samples from 3,890 Czech army
recruits and testing them for toxoplasmata. The recruits were
monitored in the following years and the number of accidents they
were involved in was recorded and analyzed. Severe toxoplasma
infection in conjunction with a particular blood group (rhesus
negative) turned out to be the highest risk factor. Blood groups can
indeed play an important role in parasite infections—some groups
offer greater protection than others.
BUT HOW DOES our lady with the razor blade fit in to all this? Why
is she not horrified by the sight of her own blood? Why is the feeling
of slicing through her skin, flesh, and nerves processed not as
painful but rather, as thrilling? How can pain have become the hot
sauce in the otherwise bland soup of her everyday life?
There are various ways of approaching this question. One of
them is to look at toxoplasmata. When we are infected with them,
our immune system activates an enzyme (IDO) to protect us from
these parasites. IDO breaks down a substance that the invaders like
to eat, forcing them to enter the less active, dormant state.
Unfortunately, this substance is also one of the ingredients needed to
produce serotonin. (Remember: a lack of serotonin is associated
with depression and anxiety disorders.)
If the brain lacks serotonin because IDO has snatched it all away
from under the parasite’s nose, our mood can be affected negatively.
In addition, nibbled-on precursors of serotonin can dock onto certain
receptors in the brain and cause symptoms like lethargy. These are
the same receptors as those targeted by painkillers—the result is
indifference and sedation. It can take quite drastic measures to drag
the brain out of that state of torpor so it can feel emotions keenly
again.
Our body is a clever body. It carries out a risk–benefit analysis.
When a parasite needs to be combated in the brain, the brain’s
owner is likely to be in a bad mood. Activating IDO is usually a kind
of compromise. The body occasionally uses this enzyme to snatch
food away from its own cells. IDO is more highly activated during
pregnancy, but only near the interface between mother and child.
There, it snatches the food away from immune cells. That weakens
them, making them react more mildly to the semi-alien presence of
the baby.
Would the lethargy triggered by IDO be enough to drive someone
to suicide? To put the question another way, what does it take to
make people think about killing themselves? Where would a parasite
need to start if it wanted to switch off our natural fear of harming
ourselves?
Fear is associated with a part of the brain called the amygdala.
Certain fibers run directly from the eyes to the amygdala, so the
mere sight of a spider can trigger an immediate reaction of fear. This
connection exists even in blind people whose visual cortex has been
damaged by an injury to the back of the head. They no longer see
the spider, but they still feel it emotionally. So, our amygdala plays a
major role in the development of fear. If the amygdala gets damaged,
a person can become fearless.
Examinations of intermediate toxoplasmata hosts show that the
apartments the toxoplasmata occupy to hibernate in are mainly
found in the muscles and the brain. Those in the brain are found in
three locations. In descending order of frequency, these are the
amygdala, the olfactory center, and the area of the brain directly
behind the forehead. As we know, the amygdala is responsible for
the perception of fear. The olfactory center could be responsible for
the rat’s new-found love of cat urine. The third area is slightly more
complex.
This part of the brain creates possibilities by the second. If a
research subject is wired up to a brain scanner and confronted with
questions about faith, personality, or morality, or if he is asked to
complete complex and challenging cognitive tasks, lively activity is
recorded in this region. One theory proposed by brain researchers is
that this indicates that this area of the brain is drawing up many
designs every second. “I could believe in the religion followed by my
parents. I could start licking the desk in front of me during this
conference. I could read a book and have a cup of tea. I could dress
the dog up in a funny costume. I could film myself singing a jolly
song. I could drive my car at breakneck speed. I could reach for that
razor blade . . .” There are hundreds of possibilities every second,
but which will win through and which will be carried out?
So, if you are a parasite with a plan, it makes sense to settle
here. From here, it might be possible to promote self-destructive
tendencies and weaken the mechanisms that suppress these
courses of action.
Researchers wouldn’t be researchers if they hadn’t come up with
the idea of repeating Joanne Webster’s experiment with human
beings. So they had humans sniff different animals’ urine. Men and
women who were toxoplasma carriers had a different reaction to the
smell of cat pee from those who were parasite-free. Men liked the
smell considerably more, women less.
Smell is one of our most basic senses. Unlike taste, hearing, or
vision, smells are not checked out before they make their way to our
consciousness. Strangely, we can dream all sensory experiences
except smells. Our dreams are always odorless. Truffle pigs know
just as well as toxoplasmata that smells can trigger an emotional
response. As it happens, the scent of a truffle is pretty similar to the
scent of a sexy truffle pig male. When an infatuated female truffle pig
smells a sexy male truffle pig hiding under the earth, she will dig and
dig until . . . she discovers a disappointingly unsexy fungus for her
owner. I think the astronomical price of truffles is more than justified
when you consider how frustrating such a find must be for a poor
sow. Anyway, the point is that smells can stimulate attraction.
Some shops exploit this phenomenon. Economists call it scent
marketing. One American clothing manufacturer even uses sex
pheromones to attract potential customers. In Frankfurt, where I live,
you can often see long lines of teenagers outside the store’s
darkened and pheromone-scented entrance. If the shopping precinct
were closer to areas with free-ranging pigs, some pretty entertaining
scenes might result.
SO, IF ANOTHER organism can make us perceive smells differently,
couldn’t it also influence other sensory impressions?
There is a well-known illness whose main symptom is false
sensory perceptions: schizophrenia. For example, people suffering
from schizophrenia might feel like an army of ants is crawling all over
their back, although there are no such insects anywhere nearby.
They hear voices and obey their commands, and they can be
extremely lethargic. About half to one percent of people suffer from
schizophrenia.
There is much about the clinical picture of schizophrenia that is
still unclear. Most drugs used to treat it do so by deactivating a signal
transmitter in the brain that is overabundant in people with
schizophrenia: dopamine. Toxoplasmata possess genes that
influence the production of dopamine in the brain. Not all people who
suffer from schizophrenia are parasite carriers—so that can be ruled
out as the sole cause—but the proportion of carriers among those
who suffer from schizophrenia is about twice that among those who
do not.
Toxoplasma gondii could, therefore, influence us via the fear,
smell, and behavioral centers of the brain. A higher risk of being
involved in an accident, attempting suicide, or suffering from
schizophrenia indicates that an infection affects at least some of us.
It will take some time before discoveries like these have
consequences for standard medical practice. Suspicions need to be
scientifically proven and further research into possible treatments is
needed. This insistence of science on time-consuming validation
processes can cost lives. Antibiotics, for example, did not appear in
our pharmacies until decades after they were discovered. But this
caution can also save lives. Thalidomide and asbestos could easily
have been tested for a little bit longer before entering the market.
Toxoplasmata can influence us far more than we would ever have
thought possible just a few years ago. And they have rung in a new
scientific age. An age in which a crude lump of cat feces can show
us how susceptible our lives are to change. An era in which we are
just beginning to understand just how complex the connections are
between us, our food, our pets, and the microscopic world in, on,
and around us.
Is this spooky? Well, maybe a little bit. But isn’t it also exciting to
see how we are gradually decoding processes that we used to
believe were part of our inescapable destiny? This could help us to
grab the risks by the horns and defy them. Sometimes, it takes
nothing more than a scoop of cat litter, a well-cooked chicken, and
properly washed fruit and veggies.
Pinworms
little white worms that like to live in our gut. Over
many centuries, they have adapted their behavior to live with us. Half
the world’s population has had a visit from these worms at some time
or other. Some people never even notice. For others, it’s an
embarrassing infestation they’d rather not talk about. If you look at
just the right moment, you can even see them giving us a wave out
of the anus. They are 0.2 to 0.4 inches (5 to 10 millimeters) long, and
white, and they sometimes have a pointed end. They look a little like
the vapor trails left by jets in the sky except they don’t get longer and
longer. Anyone who has a mouth and a finger can get these
parasites, which are also known as threadworms. Finally, there’s an
advantage to being fingerless and/or mouthless!
Let’s put the cart before the horse, or rather, the worm. A ladyworm looking for a place to lay her eggs wants to make sure they will
have a secure future. And such a place is not so easy to reach. A
pinworm egg has to be swallowed by a human being, then hatch in
the small intestine so that it can reach the large intestine by the time
it is a grown-up worm. But our mother-worm-to-be lives in the lower
reaches of the digestive tract with everything moving in the wrong
direction for her needs. So she wonders how she is ever going to get
back to her host’s mouth to give her eggs the start in life that they
need. Here she makes use of the only kind of intelligence such a
creature has at her disposal—the intelligence of adaptation. Whether
this is the origin of the word “brown noser” or not is open to question.
Female pinworms know when we are still, lying down, and too
comfortable to rouse. That’s exactly when they set off toward the
anus. They lay their eggs in the many little creases around the anus
and wriggle around until it starts to itch. They then slip quickly back
inside the gut, because experience has taught them that soon a
THERE ARE SOME
hand will appear and finish off the job. Under the bedclothes, the
hand heads for the backside, targeting that itch. The same neural
pathways that passed on the itch now give the instruction to scratch.
We obey the instruction, thereby providing the pinworm’s children
with an express connection to the mouth area.
When are we least likely to go and wash our hands after
scratching our behind? When we are oblivious to all this action
because we are asleep or too sleepy to get up and head for the
bathroom. And that is pinworm egg-laying time. It’s clear what that
next dream about sticking your finger in a yummy chocolate cake will
mean. It will mean that those eggs are heading to their ancestral
home: your mouth. That might sound gross, but it’s not so very
different from eating chickens’ eggs. Only chickens’ eggs are bigger
and usually cooked.
Organisms that move into our gut uninvited and implement their
plans for progeny there get a bad rap from us. And we often avoid
talking about them with others. It’s as if we feel we have been a bad
manager for our body, failing to lay down the law properly and letting
any old strangers take up residence without interviewing them first.
But pinworms are not just any old strangers. They are guests who
wake the manager in time for morning exercises and then give their
host a massage to stimulate the immune system. Furthermore, they
steal very little of our food.
It is not good to keep these parasites as permanent guests, but
once in a lifetime is fine. Scientists suspect that when kids have had
worms, they are less likely to contract severe asthma and diabetes in
later life. So welcome, Mr. and Mrs. Pinworm, come on in! But don’t
outstay your welcome, please. An uncontrolled attack of worms can
have three rather unwelcome consequences.
1. Lack of a good night’s sleep can lead to concentration problems,
nervousness, or irritability during the day.
2. What the worms don’t want is to lose their way—and we don’t
want them to either. When worms get into places they don’t
belong, they have to go. Who wants a pinworm with a bad sense
of direction, after all?
3. Sensitive guts, or those containing overactive worms, can
become irritated. Worms have a tendency to cause irritation
anyway. There are many problems this can cause: not going to
the toilet often enough, going to the toilet too often, abdominal
cramps, headaches, nausea, or none of the above.
If a worm host has any of these symptoms, a visit to the doctor is
essential! The doctor will ask you to put sticky tape to a use you
never learned in arts and crafts lessons in elementary school. Some
doctors are more charming about it than others, but, in essence,
what they will tell you to do is to spread your cheeks, stick tape to
your anus and the surrounding area, pull it off again, bring it to the
surgery, and hand it over to the receptionist.
Worm eggs are small and round and adhere well to sticky tape.
Searching for eggs on Easter Sunday morning would be a lot more
efficient if you had a great big egg-magnet that attracted all the eggs
from the garden. Since worm eggs are so much smaller than Easter
eggs, it makes sense to use a trick like this. The sticky-tape egg hunt
has to take place in the morning, as that’s when most eggs are there.
And it is not a good idea to flush out or sweep clean the worm
garden before you hunt for the eggs. So the first thing that comes
into contact with the region in the morning should be those strips of
sticky tape.
The doctor will examine the fruits of your labors under the
microscope, hunting for little oval eggs. If they are already
developing into larvae, they will have a line down the middle. The
doctor can then prescribe the right medication and your pharmacist
will help you win the battle to get rid of your unwanted guests. The
typical medication prescribed—let’s call it mebendazole for the sake
of argument—works on the tit-for-tat principle we all know from
kindergarten: if you bother my gut, I’ll bother yours.
The medication makes its way from mouth to rectum and meets
our renegade squatters along the way. Mebendazole is much more
harmful to a worm’s gut than it is to ours. It places the worms on a
forced diet, denying them all access to sugar. Sugar is the stuff of life
for worms, so this will be the last diet they ever go on. It’s a bit like
trying to get rid of unwanted guests by not offering them anything
more to eat.
Pinworm eggs live for a long time. If you have worms and can’t
keep your hands away from your mouth, you should at least try to
reduce the number of eggs in the area to a minimum. Bedclothes
and underwear should be changed every day and washed at 140
degrees Fahrenheit (60 degrees Celsius) or hotter, regular hand
washing is essential, and intense itching might be better treated with
creams than by scratching. My mother is convinced that worms can
be eliminated by swallowing a whole clove of garlic once a day. I
have not been able to find any scientific studies to prove this, but nor
are there any studies about what temperature necessitates the
wearing of warm jackets and my mother is always right about that! If
all this fails, do not despair. Go back to your doctor and be proud of
having such an inviting gut.
Of Cleanliness and Good Bacteria
WE ALWAYS WANT to protect ourselves from harm. Few people would
choose to have Salmonellae or a nasty H. pylori. Even though we
have not yet identified them all, we know already that we’d rather not
have chubby bacteria or microbes that cause diabetes or
depression. Our greatest protection against them is cleanliness. We
are careful about eating raw food, kissing strangers, and washing
our hands to rid them of anything that might spread disease. But
cleanliness is not always what we imagine it to be.
Cleanliness in our gut is something akin to cleanliness in a forest.
Even the most conscientious of cleaners would not dream of taking a
mop to the forest floor. A wood is clean if the beneficial plants it
contains are in healthy equilibrium. We can help the forest along by
sowing seeds and hoping new plants will take root. We can identify
favorite or useful plants in the forest and nurture them to help them
grow and multiply. Sometimes, there are nasty pests. Then, careful
consideration is in order. If the situation is desperate, chemicals
might be the answer. As their name implies, pesticides are great at
killing pests, but it is not a great idea to spray them round like air
freshener.
Clever cleanliness begins with our everyday routines—but what
is well-advised caution and what is excessive hygiene? There are
three main tools for keeping our insides clean. Antibiotics can rid us
of acute pathogens, while prebiotic and probiotic products can
promote beneficial elements. Pro bios means “for life.” Probiotics are
edible living bacteria that can make us healthier. Pre bios means
“before life.” Prebiotics are foodstuffs that pass undigested into the
large intestine, where they feed our beneficial bacteria so that they
thrive better than bad bacteria. Anti bios means “against life.”
Antibiotics kill bacteria and are our saviors when we have picked up
a pack of bad bacteria.
Everyday Cleanliness
about cleanliness is that it is mostly in the
head. A peppermint tastes fresh, clean windows look clear, and we
love slipping into a freshly made bed after a hot shower. We like the
smell of clean things. We like to run our hands over smooth, polished
surfaces. We find comfort in the idea that we are protected from an
invisible world of germs if we use enough disinfectant.
In Europe 130 years ago, it was discovered that tuberculosis is
caused by bacteria. This was the first time the public took notice of
bacteria—and they were seen as bad, dangerous, and, most
worryingly, invisible. It was not long before new regulations were
introduced in European countries: patients were isolated so they
could not spread their germs; spitting was forbidden in schools; close
physical contact was discouraged; and warnings were issued against
“the communism of the towel!” People were even advised to limit
kissing to “the erotically unavoidable.” That might sound funny to us
today, but those ideas put down deep roots that can still be felt in our
modern Western society: spitting is still frowned upon, we are still
reluctant to share towels and toothbrushes, and we keep a greater
physical distance in our dealings with others than most cultures.
Preventing deadly disease by banning pupils from spitting at
school seemed like a simple and effective idea. We internalized it in
our culture as a social rule. Those who did not comply were
THE FASCINATING THING
despised as a danger to everyone’s health. This attitude was passed
on from parent to child, and public spitting became a social taboo.
Cleanliness really was thought to be next (in importance) to
godliness; people craved a sense of order in a life full of chaos. The
anthropologist Mary Douglas summed this up in her book Purity and
Danger with the phrase, “Dirt is matter out of place.”
Bathing as a way of keeping the body clean was a privilege of the
rich even up to the beginning of the twentieth century. It was around
that time that dermatologists in Germany began to call for “a bath a
week for every German!” Large companies built bathhouses for their
employees and encouraged personal hygiene by issuing them with
free towels and soap. The tradition of the weekly bath did not really
take hold until the 1950s. Then, typical families took their bath on a
Saturday evening, one after another in the same bathwater, and
hard-working Dad often got to go in the tub first. Originally, personal
cleanliness meant ridding the body of unpleasant smells and visible
dirt. As time went on, this concept became increasingly abstract. It’s
hard for us today to imagine this once-a-week family bathing routine.
We spend money on disinfectants to get rid of things we can’t even
see. The surface in question looks exactly the same after cleaning
as it did before—yet just knowing it is clean is extremely important to
us.
The news media tell us horror stories about dangerous flu
viruses, multi-drug-resistant superbugs, and EHEC-contaminated
food. When food contamination scares such as tainted salad recalls
are in the news, some people react by giving up lettuce while others
type “full body decontamination shower” into Google. Different
people deal with fear in different ways. Dismissing this as hysteria is
too easy. It makes more sense to try and understand where these
fears come from.
Fear-driven hygiene involves attempting to clean everything away
or kill it off. We don’t know what it might be, but we assume the
worst. When we clean obsessively, we do indeed get rid of
everything—both bad and good. This cannot be a good kind of
cleanliness. The higher the hygiene standards in a country, the
higher that nation’s incidence of allergies and autoimmune diseases.
The more sterile a household is, the more its members will suffer
from allergies and autoimmune diseases. Thirty years ago, about
one person in ten had an allergy. Today that figure is one in three. At
the same time, the number of infections has not fallen significantly.
This is not smart hygiene. Research into Nature’s huge range of
bacteria has led to a new understanding of what cleanliness should
mean. It is no longer defined as the attempt to kill off potential
dangers.
More than 95 percent of the world’s bacteria are harmless to
humans. Many are extremely beneficial. Disinfectants have no place
in a normal household. They are appropriate only if a family member
is sick or the dog poops on the carpet. If a sick dog poops on the
carpet, there are no holds barred—bring on the steam cleaners,
disinfectant by the bucket-load, or a small flame thrower, perhaps.
That might even be fun! But if the floor is just covered in dirty
footprints, water and a drop of cleaning fluid are all you need. That
combination is already enough to reduce the bacteria population of
your floor by 90 percent, and it leaves the normal, healthy population
of the floor a chance to recolonize the territory. What remains of any
harmful elements is so little as to be negligible.
The aim of cleaning, then, should be to reduce bacteria numbers
—but not to zero. Even harmful bacteria can be good for us when
the immune system uses them for training. A couple of thousand
Salmonella bacteria in the kitchen sink are a chance for our immune
system to do a little sightseeing. They become dangerous only when
they turn up in greater numbers. Bacteria get out of hand when they
encounter the perfect conditions: a protected location that is warm
and moist with a supply of delicious food. There are four
recommended strategies for keeping them in check: dilution,
temperature change, drying, and cleaning.
Dilution
technique we also use in the laboratory. We dilute
bacteria with fluids and administer drops with different concentrations
of bacteria to wax moth larvae, for example. Wax moth larvae
change color when they get sick. That makes them a good indicator
of the concentration of bacteria required to cause illness. For some,
it’s a little as a thousand per drop of fluid, for others, as many as ten
million.
One example of bacteria dilution in the home is washing fruit and
vegetables. Washing dilutes most soil-dwelling bacteria to such a low
concentration that they become harmless to humans. Koreans add a
little vinegar to the water to make it slightly acidic and just that bit
more uncomfortable for any bacteria. Airing a room is also a dilution
technique.
If you dilute the bacteria on your plates, cutlery, and cutting board
nicely with water, then wipe them over with a kitchen sponge before
putting them away, you may as well have licked them clean with your
tongue. Kitchen sponges offer the perfect home for any passing
microbe—nice and warm, moist, and full of food. Anyone looking at a
kitchen sponge under the microscope for the first time usually wants
to curl up on the floor in a fetal position, rocking back and forth in
disgust.
Kitchen sponges should only be used for cleaning the worst of
the dirt off. Plates, cutlery, and so on should then be rinsed briefly
under running water. The same is true for dish towels or drying-up
cloths if they never get a chance to dry out. They are more useful for
spreading a nice even layer of bacteria on your utensils than for
DILUTION IS A
drying them. Sponges and cloths should be thoroughly wrung out
and allowed to dry—otherwise they become the perfect place for
moisture-loving microbes.
Drying
on dry surfaces. Some cannot survive there
at all. A freshly mopped floor is at its cleanest after it has dried.
Armpits that are kept dry by antiperspirants are less cozy homes for
bacteria—and fewer bacteria produce less body odor. Drying is a
great thing. If we dry food it keeps for longer before it rots. We use
this to our advantage: just think of foodstuffs like pasta, muesli, crisp
bread, dried fruit (such as raisins), beans, lentils, and dried meats.
BACTERIA CANNOT BREED
Temperature
of the world, the environment is refrigerated naturally
once a year. From a bacteriological point of view, winter is the real
spring clean! Refrigerating food is an extremely important part of our
daily lives, but a fridge contains so much food that it remains a
paradise for bacteria even at low temperatures. The optimum
temperature for your fridge is something below 41 degrees
Fahrenheit (5 degrees Celsius).
Let’s move on to another household appliance—the washing
machine. Most washing machine programs use the dilution principle
to clean our clothes and that is sufficient. However, damp kitchen
cloths, a load of underpants, or sick people’s laundry should be
washed at 140 degrees Fahrenheit (60 degrees Celsius) or more.
Most E. coli bacteria are killed by temperatures above 104 degrees
Fahrenheit (40 degrees Celsius), and 158 degrees Fahrenheit (70
degrees Celsius) is enough to kill off tougher Salmonella bacteria.
IN MANY PARTS
Cleaning
a film of fats and proteins from surfaces.
Any bacteria living in it or under it will be removed along with the film.
We usually use water and cleaning fluid to achieve this. Cleaning is
the technique of choice for all living spaces, kitchens, and
bathrooms.
This technique can be taken to the absolute extreme. That is
sensible when you are manufacturing medical drugs that are
destined to be pumped straight into a patient’s veins (such as
infusions). The drugs need to be absolutely free of all bacteria. This
is achieved in pharmacological laboratories by using iodine, for
example. Iodine sublimates, which means it transitions from a solid,
crystalline state to a gaseous vapor in the presence of heat without
passing through a liquid phase. So pharmacologists heat up iodine
until the entire production lab is veiled in a blue vapor.
It sounds like the simple principle of the steam cleaner, but there
is more to it than that. Iodine can also desublimate. To make this
happen, the room is cooled and the vapor immediately recrystallizes.
Millions of tiny crystals form on all surfaces and even in mid-air,
trapping every microbe as they do so, locking them up in a crystal
prison as they fall to the ground. Workers pass through several
airlocks and disinfection chambers, dress up in germ-free bodysuits,
and sweep up the iodine crystals.
In principle, we use the same system when we use hand cream.
We trap microbes in a film of fat and hold them captive there. When
we wash the film off, we rinse the bacteria away with it. Since our
skin produces a natural coating of fat, soap and water are often
enough to achieve this effect. Some of the fat layer remains, aiding
its replenishment after washing. Too frequent hand washing makes
no sense—and the same is true of too frequent showering. If the
CLEANING MEANS REMOVING
protective fat layer is rinsed away too often, our unprotected skin is
exposed to the environment.
Bacteria trapped in iodine crystals.
That gives odor-producing bacteria a better foothold, making us
smell more pungently than before, creating a vici ous circle.
New Methods
Ghent in Belgium is currently trying out a brand-new
method. The researchers are attempting to use bacteria to combat
body odor. They disinfect volunteers’ armpits, spread them with
odorless bacteria, and start the stopwatch. After a couple of minutes,
the subjects are allowed to put their shirts back on and go home.
The volunteers return repeatedly to the laboratory, where experts
sniff their armpits. The initial results are quite promising—the
odorless bacteria manage to banish their smelly colleagues in many
of the subjects’ armpits.
Not far away, across the border in Germany, the same method is
in use in the public toilets of the small town of Düren. A company is
using a mixture of bacteria to clean the toilets. The odorless bacteria
occupy the places normally colonized by the bugs that create that
all-too-familiar public toilet smell. The idea of using bacteria to clean
public conveniences is a brilliant one. Unfortunately, the company
refuses to reveal the recipe for its cocktail of bacterial cleaners, so a
scientific evaluation is impossible. However, the town of Düren
seems to be faring very well with this experiment.
These new ideas about the use of bacteria illustrate one thing
very clearly: cleaning does not mean annihilating all bacteria.
Cleanliness is a healthy balance of sufficient good bacteria and a few
bad ones. That means smart protection against real dangers and,
sometimes, deliberate contamination with good bugs. With this in
A TEAM FROM
mind, we can perhaps better appreciate the wisdom of observations
like that of the American writer Suellen Hoy, who says in her book
Chasing Dirt, “From the perspective of a middle-class American
woman (also a seasoned traveler) who has weighed the evidence, it
is certainly better to be clean than dirty.”
Antibiotics
killers of dangerous pathogens. And their
families. And their friends. And their acquaintances. And distant
acquaintances of their acquaintances. That makes them the best
weapon against dangerous bacteria—and the most dangerous
weapon against good bacteria. But who is it who manufactures most
antibiotics? It’s bacteria. Huh?
Antibiotics are the weapons used by both sides in the war
between fungi and bacteria.
Ever since researchers discovered all this, pharmaceutical
companies have been intensively farming bacteria. Huge tanks with
a capacity of up to 26,500 US gallons (100,000 liters) are used to
grow so many bacteria that their numbers can hardly be expressed
in any meaningful figures. They produce antibiotics, which we purify
and press into little tablets. The product sells well, especially in the
United States. When researchers were planning a study of the effect
of antibiotics on the flora of the gut, they were able to find only two
people in the entire San Francisco Bay Area who had not taken
antibiotics in the previous two years. In Germany, one person in
every four takes antibiotics once a year on average. The main
reason for taking them is colds. This is like a knife in the heart of any
microbiologist. Colds are often not even caused by bacteria, but by
viruses! Antibiotics can work in three different ways: by peppering
ANTIBIOTICS ARE RELIABLE
the bacteria with holes, by poisoning the bacteria, or by rendering
the bacteria unable to reproduce. They have no effect on viruses at
all.
So taking antibiotics to cure a cold is usually a complete waste of
time. If they do bring about an improvement, this is due either to the
placebo effect or to the work of the immune system in combating the
cold virus. The senseless use of antibiotics does, however, kill many
helpful bacteria, which can be harmful in itself. To avoid this, doctors
can perform a procalcitonin test, which indicates whether cold-like
symptoms are caused by a bacterial or viral infection. The test can
be especially helpful to make sure children don’t take antibiotics
unnecessarily.
There is no reason not to take antibiotics when it is medically
appropriate to do so. The benefits certainly outweigh the
disadvantages, for example, in cases of severe pneumonia or for
helping children get over a particularly bad infection with no longterm damage. In such cases, those little tablets can save lives.
Antibiotics stop bacteria from reproducing, the immune system kills
off any remaining pathogens, and we soon start to feel better. We
have to pay a price for this, but in the final reckoning, it’s a good
deal.
The most common side effect is diarrhea. Even those who don’t
get diarrhea may notice that they leave a rather larger deposit in the
morning toilet bowl than usual. To tell it like it is: a large portion of
that pile is dead gut bacteria. The antibiotic tablet does not travel
directly from mouth to blocked-up nose. It descends into the stomach
and then on to the gut. Before it graduates from there into the
bloodstream—and then to the nose, among other places—it peppers
our microbe collection with holes, poisons our gut bacteria, and
makes them sterile. The result is a formidable battlefield—you can
see the casualties the next time you go to the toilet.
Antibiotics can alter our gut flora significantly. Our microbe
collection becomes much less diverse and the abilities of the
bacteria in it can change. Changes include the amount of cholesterol
they can absorb, their ability to produce vitamins (like skin-friendly
vitamin H), and the type of foodstuffs they can help us digest.
Preliminary studies carried out at Harvard and in New York have
shown that the two antibiotics metronidazole and gentamicin cause
particularly hefty changes in the flora of the gut.
Antibiotics can be problematic for children and old people. Their
gut flora is already less stable and less able to recover after
treatment with antibiotics. Research in Sweden showed that the gut
bacteria of children were still significantly altered two months after
taking antibiotics. Their guts contained more potentially harmful
bacteria and fewer beneficial types like Bifidobacteria and
Lactobacilli. The antibiotics used were ampicillin and gentamicin.
The study involved only nine children, which means it is not
particularly meaningful in scientific terms, but it remains the only
study of its kind so far. So the results should be accepted with a
degree of caution.
A more recent study of pensioners in Ireland revealed a clear
dichotomy. Some gut landscapes recovered very well after a course
of antibiotics, while others remained permanently altered. The
reasons for this are still completely unclear. The ability to return
quickly to a stable state following an extreme experience is
described with same word by gut researchers and psychologists:
resilience.
Even though antibiotics have been in use for more than fifty
years, studies of the long-term effects can still be counted almost on
one hand. The reason for this is technological: the equipment
necessary for such investigations has only been around for a couple
of years. The only long-term effect that has been scientifically proven
is drug resistance. For as long as two years after taking antibiotics,
bad bacteria are still present in the gut, telling their great-great-great. . . -grandchildren stories about the war.
These are the ones that resisted the antibiotics and survived. And
with good reason. Bacteria develop resistance strategies. Some
install tiny pumps in their cell walls to pump the antibiotic out like
emergency workers pumping water out of a flooded cellar. Others
prefer to disguise themselves so the antibiotics cannot recognize
their surface and so cannot pepper them with holes. Yet others use
their ability to split things—they build tools to cut the antibiotics to
pieces.
The thing is that antibiotics rarely kill all bacteria. They kill certain
communities depending on the toxins they use. There will always be
some bacteria that survive and become experienced fighters. In the
case of serious illness, these fighters can become a problem. The
more resistances the bacteria have developed, the more difficult it is
to get them under control again with antibiotics.
Every year, many thousands of people die because they are
infected with bacteria that have developed resistances that no drug
can counter. When their immune system is compromised—for
example, after an operation—or if the resistant bacteria have got out
of hand after a long course of treatment with antibiotics, the patient
can be in real danger. Very few new drugs are in development, for
the simple reason that it is not very profitable for pharmaceutical
companies to do so.
SO HERE ARE four pieces of advice for anyone who wants to keep
out of unnecessary antibiotic gut wars.
1. Do not take antibiotics unless it is really necessary. And if you do
have to take them, then always complete the course. This is
because resistance fighters who are less skilled will eventually
give up the cause and succumb to the drug. So the only ones that
remain are those that would never have been killed by the
antibiotics anyway. But at least the rest will have been well and
truly done in.
2. Choose organically farmed meat. Drug resistances differ from
country to country. It is shocking to see how often these
resistances correspond to the antibiotics used in large-scale
animal farming. In countries like India or Spain, for example, there
is almost no regulation of the amount of antibiotics given to
animals. This turns the animals’ guts into giant breeding zoos for
resistant bacteria. And people in such regions have significantly
more infections with multi-drug-resistant strains. In other
countries, regulations do exist, but even here the rules are
ridiculously vague. This allows many vets to make a lot of money
in the semi-legal antibiotics trade.
It was not until 2006 that the European Union banned the use
of antibiotics in animal feed as performance enhancers. The kind
of performance being enhanced here is the ability of an animal to
not die of infections in a crowded and dirty pen. Antibiotics are a
great way to “enhance” this “performance.” In the United States,
the Food and Drug Administration is working on a voluntary plan
to phase out the use of some of these antibiotics in regular
farming. In organic farming, the Department of Agriculture forbids
the use of any antibiotics, and an animal given antibiotics—for
example, to relieve suffering—must be removed from organic
production.
If possible, it is worth spending that little extra—to prevent
resistance-breeding zoos and for your peace of mind . . . and
peace of gut. The dividends are not immediate, but it is an
investment in a better future for us all.
3. Wash fruit and vegetables thoroughly. Animal feces are a popular
fertilizer, and liquid manure is used in vegetable fields. In many
countries, fruit and vegetables are not routinely tested for
residues of antibiotics—and certainly not for multi-drug-resistant
gut bacteria. Milk, eggs, and meat are usually tested to make sure
they don’t exceed certain limits. So err on the side of caution and
wash your fruit and vegetables one extra time if you are not sure.
Even tiny amounts of antibiotics can help bacteria develop
resistances.
4. Take care abroad. One traveler in four returns home carrying
highly resistant bacteria. Most disappear in a few months, but
some lurk around for much longer. Special care should be taken
in bacterial problem countries like India. In Asia and the Middle
East, you should wash your hands regularly, and clean fruit and
vegetables thoroughly—if necessary with boiled water. Southern
Europe also has its problems. “Cook it, peel it, or leave it” is not
only a good rule for avoiding diarrhea, it also protects against
unwanted resistant souvenirs for you and your family.
Are There Alternatives to Antibiotics?
that have functioned for centuries without
causing resistances. (Fungi, such as the penicillin fungus, are not
plants but opisthokonts, like animals.) When parts of plants snap off
or become perforated, they need to produce antimicrobial
substances at the location of the damage. If they did not do this, they
would immediately become a feast for any bacteria in the vicinity.
Pharmacies sell concentrated plant antibiotics to treat developing
cold symptoms, urinary infections, and inflammations in the mouth
and throat. Some products contain mustard seed or radish seed oil,
for example, or chamomile and sage extract. Some can reduce the
numbers of viruses as well as bacteria. That leaves our immune
system with less to contend with, giving it a better chance of dealing
with pathogens.
PLANTS PRODUCE ANTIBIOTICS
Such plant-based remedies are not the solution for serious
illnesses or for illnesses that drag on with no noticeable
improvement. In such cases, they can even be harmful because they
encourage us to wait too long before turning to powerful antibiotics.
In recent years, the incidence of heart and ear damage in children
has increased. This is often due to the behavior of parents who want
to protect their children from too much exposure to antibiotics. Such
a decision can have damaging consequences. A well-informed
doctor will not prescribe antibiotics for every little thing—but will tell
you in no uncertain terms when they are really necessary.
Our relationship with antibiotics is an arms race: we use them to
arm ourselves to the hilt when faced with dangerous bacteria, and
they respond by arming themselves with even more dangerous
resistances. Medical researchers should really be developing the
next generation of weapons in this race. Every one of us accepts a
trade-off when we take these drugs. We agree to sacrifice our good
bacteria in the hope of getting rid of the bad. In the case of a minor
cold, that’s not a good deal; for serious illnesses, it’s a trade that
pays off.
There is no species protection program for gut bacteria. We can
be pretty certain that we have annihilated many family heirlooms
since the discovery of antibiotics. The places they leave vacant
should be colonized by the best candidates possible—probiotics, for
example. They help the gut to return to a state of healthy equilibrium
after danger has been averted.
Probiotics
billions of living bacteria every day. They are on
raw food, a few survive on cooked food, we nibble on our fingers
WE SWALLOW MANY
without even thinking about it, we swallow our own mouth bacteria or
kiss our way through the bacterial landscapes of others. A small
proportion even survive the acid bath of the stomach and the
aggressive digestive process to reach our large intestine alive.
No one knows the majority of these bacteria. They presumably
do us no harm, or perhaps even benefit us in some way we have not
yet discovered. A few are pathogens, but they usually cannot harm
us because their numbers are just too small. Only a fraction of these
bacteria have been thoroughly checked out by scientists and given
the official seal of approval. These bacteria can proudly call
themselves probiotics.
We often read the word “probiotic” on the yogurt we find on our
supermarket shelves without having any real idea what it means or
how they work. Most will recall television commercials telling us they
strengthen our immune system, or showing us a constipated aunt
relieved of her woes and recommending this brand to everyone she
knows. That all sounds good. You don’t mind spending a little extra
for a healthy product like that. And before you know it, those
probiotics are in your shopping basket, then in your fridge, and
eventually in your mouth.
People have been eating probiotic bacteria since time
immemorial. Without them, we would not exist. A group of South
Americans had to learn that through bitter experience. They had the
clever idea of taking pregnant women to the South Pole to have their
babies. The plan was that the babies born there could stake a claim
to any oil future reserves as natives of the region. The babies did not
survive. They died soon after birth or on the way back to South
America. The South Pole is so cold and germ-free that the infants
simply did not get the bacteria they needed to survive. The normal
temperatures and bacteria the babies encountered after leaving the
Antarctic were enough to kill them.
Helpful bacteria are an important part of our life, and we are
constantly surrounded and covered by them. Our ancestors had no
idea of their existence, but they intuitively did the right thing:
protecting their food from the bacteria that make it rot by handing it
over to the care of good bacteria. In other words, they used bacteria
to preserve their food. Every culture in the world includes traditional
dishes that rely on the help of microbes for their preparation.
Germany has its sauerkraut, pickled gherkins, and sourdough
pretzels; the French love their crème fraîche; the Swiss have their
hole-riddled cheese; salami and preserved olives come from Italy;
Turks swear by a salty yogurt drink called ayran. None of these
delicacies would exist if it weren’t for microbes.
There are many, many examples from Asian cuisine: soy sauce,
kombucha drinks, miso soup, Korean kimchi. Indians have lassi and
Africans have fufu . . . the list is endless. All these foods rely on
bacteria for a process we call fermentation. The process often
results in the production of acid, which makes the yogurt or
vegetables taste sour. This acid, along with the many good bacteria,
protects the food from dangerous microbes. Fermentation is the
oldest and healthiest way of preserving food.
The bacteria used in this technique were as varied around the
world as the foods they helped to produce. The soured milk drunk in
rural Germany was made using different bacteria from those used to
make the ayran enjoyed in Anatolia. In the warmer countries of the
south, bacteria were used that prefer to work under higher
temperature conditions; in the chilly north, bacteria were chosen that
like to do their job at room temperature.
Yogurt, soured milk, and other fermented products came about by
accident. Someone left the milk outside, bacteria found their way into
the churn (either directly from the cow or from the air during milking),
the milk thickened, and a new kind of food had been invented. If a
particularly delicious yogurt bacteria jumped into the mix, people
added a spoonful of that yogurt to the next batch to make more of
the same. Unlike today’s yogurt products, however, traditional types
were the work of whole teams of different bacteria—not just selected
individual species.
The diversity of bacteria in fermented foods has fallen sharply.
Industrialization has resulted in standardized production processes
using single bacteria species isolated in laboratories. Today, milk is
briefly heated soon after it leaves the udder to kill off any potential
pathogens, but this also kills any potential yogurt bacteria. That’s
why you can’t just leave modern shop-bought milk to go sour in the
hope that it will eventually turn into yogurt.
Many foods that used to be full of bacteria are now preserved
using vinegar, as is the case with most pickled gherkins today. Some
things are fermented using bacteria but then heated to kill off the
microbes—shop-bought sauerkraut, for instance. Fresh sauerkraut is
usually only sold in specialist health-food stores these days.
Scientists in the early twentieth century suspected that good
bacteria were of great benefit to us. That is when Ilya Metchnikoff
appeared on the yogurt scene. The Nobel Prize winner spent his
time observing Bulgarian mountain peasants. He realized they often
lived to be a hundred years old or more, and they were unusually
contented. Metchnikoff suspected the key to their longevity lay in the
leather bags they used to transport the milk from their cows. The
peasants had to walk long distances, and their milk often turned sour
or transformed into yogurt in the bags before they reached home.
Metchnikoff became convinced that the secret to their long lives was
their regular consumption of this bacterial product. In his book The
Prolongation of Life, he asserted the claim that good bacteria can
help us live longer, better lives. From then on, bacteria were no
longer just anonymous components of yogurt, but important
promoters of health. However, Metchnikoff’s timing could hardly have
been worse. Shortly before, it had been discovered that bacteria
cause disease. Although the microbiologist Stamen Grigorov
identified the bacterium described by Metchnikoff as Lactobacillus
bulgaricus in 1905, he soon turned his efforts to the fight against
tuberculosis. The successful use of antibiotics in fighting disease
from around 1940 meant that the idea was fixed in most people’s
minds: the fewer bacteria, the better.
We have babies to thank for the fact that Ilya Metchnikoff’s idea
and Grigorov’s bacillus eventually found their way onto our
supermarket shelves. Mothers who were unable to breast-feed their
babies found they often had a problem with their bottle-fed offspring.
The babies were getting diarrhea much more often than they should.
This took the formula-milk industry by surprise, because they had
taken care to make sure their product contained the same
substances as real breast milk. What could be missing? The answer
was, of course, bacteria. And, specifically, the bacteria that live on
milky nipples and which are particularly common in the guts of
breast-fed babies: Bifidobacteria and Lactobacilli. These bacteria
break down the sugar in milk (lactose) and produce lactic acid
(lactate), so they are classified as lactic-acid bacteria. A Japanese
scientist used Lactobacillus casei Shirota to create a special yogurt,
which mothers could initially buy only in pharmacies. When they fed
it to their babies every day, the infants contracted diarrhea much less
frequently. Industrial food research returned to Metchnikoff’s idea—
with baby bacteria and more modest aims.
Most normal yogurt contains Lactobacillus bulgaricus, although it
is not necessarily precisely the same sort as that in the yogurt of the
Bulgarian peasants. Today, the species discovered by Stamen
Grigorov is more correctly known as Lactobacillus helveticus spp.
bulgaricus. These bacteria are not particularly good at resisting
digestion and only a small number of them reach the large intestine
alive. That is not so important for some effects on the immune
system—often just the sight of a few empty bits of bacteria wall is
enough to prompt our immune cells into action.
Probiotic yogurt contains bacteria that researchers were inspired
to use by the case of the bottle-fed babies with diarrhea. They are
meant to reach the large intestine alive. Examples of bacteria that
can resist being digested are Lactobacillus rhamnosus, Lactobacillus
acidophilus, and the abovementioned Lactobacillus casei Shirota.
The theory is that a living bacterium will have a greater effect on the
gut. There are studies that show their effects, but they are not
sufficient to satisfy the European Food Safety Authority. It has
banned companies like Yakult and Danone from claiming their
products promote health in their advertising.
These doubts are compounded by the fact that it is not always
possible to know whether enough probiotic bacteria are reaching the
large intestine alive. A break in the cold chain, or a person with a
particularly acidic stomach or slow digestion, might kill off these
microbes before they reach their intended destination. That is not
harmful, of course, but it means consuming a probiotic yogurt may
have no effect that a normal yogurt doesn’t also have. To make any
difference to the huge ecosystem in our gut, about a billion (109)
bacteria need to make it through the system and arrive there intact.
To summarize: any yogurt can be good for you, although not
everyone can tolerate milk protein or too much animal fat. The good
news is that there is a world of probiotics beyond yogurt.
Researchers are busy in their laboratories examining selected
bacteria. They dribble bacteria directly onto gut cells in petri dishes,
feed mice with microbial cocktails, or get volunteers to swallow
capsules full of living microorganisms. Probiotic research has
roughly defined three areas in which our good bacteria can display
fascinating abilities.
1. Massaging and Pampering
take good care of our gut. They possess
genes that enable them to produce small fatty acids like butyrate.
This soothes and pampers the villi in the gut. Pampered villi are
much more stable and likely to grow bigger than unpampered ones.
The bigger the villi grow, the better they are at absorbing nutrients,
minerals, and vitamins. The more stable they are, the less rubbish
they let through. The result is that our body receives more nutrients
and fewer damaging substances.
MANY PROBIOTIC BACTERIA
2. Security Service
our gut—it is, after all, their home and they do
not willingly surrender their territory to bad bacteria. Sometimes they
defend the gut by occupying the very places pathogens like to infect
us most. When a bad bacterium turns up, it finds them sitting in its
favorite spot with satisfied grins on their faces and their handbags on
the seats next to them, leaving no room for anyone else to take up
residence. Should that signal not be explicit enough—no problem!
Security service bacteria have more tricks up their sleeves. For
example, they can produce small amounts of antibiotics or other
defensive substances that drive unfamiliar bacteria out of their
immediate vicinity. Or they use various acids, which not only protect
yogurt and sauerkraut from rotting bacteria, but also make our gut a
less inviting environment for bad bacteria. Another trick is to snatch
the bad bacteria’s food away (anyone with siblings may be familiar
with this strategy). Some probiotic bacteria seem to have the ability
to steal bad bacteria’s food from right under their noses. Eventually,
the bad guys have had enough and give up.
GOOD BACTERIA DEFEND
3. Good Advice and Training
not least, the best experts in all things bacterial are
bacteria themselves. When they work together with our gut and its
immune cells, they provide us with insider information and useful
advice. What do the different bacteria’s outer walls look like? How
much protective mucus is needed? What quantity of bacterial
defense substances (defensins) should the gut cells produce? Does
the immune system need to be more active in its reaction to foreign
substances or should it sit back and accept newcomers?
A healthy gut contains many probiotic bacteria. We benefit every
day and every second from their abilities. But sometimes our
bacterial community faces attack. That can be from antibiotics, a bad
diet, illness, stress, and many, many other causes. Our guts are then
less well cared for, less protective, and less good at giving advice.
When that is the case, we can be thankful that some of the results of
laboratory research have made it onto pharmacy shelves. Living
bacteria are available that can be used like temporary workers
brought in to help during times of heavy workloads.
Good for treating diarrhea. This is the number-one use for
probiotics. Gastroenteritis (stomach flu) and diarrhea caused by
taking antibiotics can be helped using various pharmacy-bought
bacteria. They can reduce the length of such a bout of diarrhea by
about a day. At the same time, unlike most diarrhea medications,
they are almost free of side effects. That means they are particularly
suitable for small children and old people. In conditions like
ulcerative colitis and irritable bowel syndrome, probiotics can
increase the intervals between diarrhea attacks or inflammatory
flare-ups.
Good for the immune system. For people who tend to get sick
often, it can be a good idea to try different probiotics, especially
when colds are rife. If that is too expensive, eating a pot of yogurt a
AND, LAST BUT
day may be enough, since bacteria don’t necessary have to be alive
to trigger some mild effects. Studies have shown that old people and
high-performance athletes, in particular, are less prone to catching
colds if they take probiotics regularly.
Possible protection against allergies. This is not as well
documented as the effect of probiotics on diarrhea or a compromised
immune system. Still, probiotics are a good option for parents of
children with an increased risk of developing allergies or
neurodermatitis. A large number of studies show they can offer
significant protection. In some studies, the effect could not be
proven, but that may be because each study used a different kind of
bacterium. Personally, I think the “better safe than sorry” approach is
appropriate here. Probiotics certainly do no harm to children with a
high risk of developing allergies. Some studies showed an
improvement in the symptoms of those already suffering from
allergies or neurodermatitis.
As well as the well-researched areas like diarrhea,
gastrointestinal disease, and the immune system, there are other
areas that are only now undergoing scientific scrutiny. Digestive
complaints, traveler’s diarrhea, lactose intolerance, obesity,
inflammatory joint disease, and diabetes are all promising areas of
research.
If you ask your pharmacist to recommend a probiotic product to
help with one of these problems (for example, constipation or
flatulence), she will not be able to give you one that has been
scientifically proven to work. The pharmaceutical industry and
academic research are equally behind in this area. What remains for
you is to try out different products for yourself until you hit upon a
bacterium that seems to help. The packaging should always include
the name of the bacteria the product contains. Try it for about four
weeks and if you see no improvement, give a different bacterium a
go. Some gastroenterologists will advise you about the kind of
bacteria that are more likely to be the ones you are looking for.
The rules are the same for all probiotics. You should try them for
about four weeks and make sure they are still within the best-before
date (otherwise sufficient bacteria may not have survived to have
any effect on the huge ecosystem of the gut). Before buying probiotic
products, you should find out whether they are intended by the
manufacturer for the complaint you are hoping to treat. Different
bacteria have different genes—some are better at advising the
immune system, others are more belligerent about ridding the gut of
diarrhea-causing bugs, and so on.
The best-researched probiotics to date are lactic-acid bacteria
(Lactobacilli and Bifidobacteria) and Saccharomyces boulardii, which
is a yeast. This yeast has not received the attention it deserves. It is
not a bacterium, so it is not one of my favorites either, but it does
have one huge advantage: as a yeast, it has absolutely nothing to
fear from antibiotics.
So, while we are massacring our entire bacteria population by
taking antibiotics, Saccharomyces can move in and set up house
without a worry in the world. It can then protect the gut from harmful
opportunists. It also has the ability to bind toxins. However, it does
cause more side effects than bacterial probiotics. For example, some
people have an intolerance to yeasts, which can cause them to
break out in a rash.
The fact that almost all the probiotics we know—give or take a
yeast or two—are lactic-acid bacteria shows how little we have yet
discovered in this area. Lactobacilli are normally less common
residents in the guts of adults, and Bifidobacteria are unlikely to be
the only health-promoting microbes present in the large intestine. At
the time of writing, there is only one other probiotic bacteria species
that is as well researched as the two mentioned above: E. coli Nissle
1917.
This strain of E. coli was first isolated from the feces of a soldier
returning from the Balkan War. All the soldier’s comrades had
suffered severe diarrhea in the Balkans, but he had not. Since then,
many studies have been carried out to show that this bacterium can
help with diarrhea, gastrointestinal disease, and a compromised
immune system. Although the soldier died many years ago,
scientists continue to breed his talented E. coli in medical
laboratories and package it up for sale in pharmacies so it can work
its wonders in other people’s guts.
There is one limitation to the efficacy of all current probiotics we
take: they are isolated species of bacteria bred in the lab. As soon as
we stop taking them, they mostly disappear from our gut. Every gut
is different and contains regular teams that help each other or wage
war on each other. When somebody new turns up, they are at the
back of the line when it comes to allocating places. So, currently,
probiotics work like hair conditioner for the gut. When you stop taking
them, the regular flora folk have to continue their work. To achieve
longer-lasting results, researchers are now looking at the possibilities
of a mixed-team strategy: taking several bacteria together, so that
they can help each other to gain a foothold in unknown territory.
They clear away each other’s waste and produce food for their
colleagues.
Some products you can buy at the pharmacy, drugstore, or
supermarket already use this strategy, with a mix of our trusty old
lactic-acid friends. And it seems they really do work better as a team.
The idea that we might be able to encourage these bacteria to settle
permanently in our gut is a nice one, but it has not yet been seen to
work well . . . to put it mildly.
But if you persist doggedly with the teamwork strategy, it can
have impressive results, for example, in treating Clostridium difficile
infections. Clostridium difficile is a bacterium that can survive
treatment with antibiotics and then colonize the entire area left free
by the bacteria killed by treatment. Infected people often have
bloody, slimy diarrhea for many years, which does not respond to
further treatment with antibiotics or probiotics. This can put great
strain not only on the body, but also on the mind.
In difficult situations like this, doctors really have to use all their
creativity. A few brave medics have now begun transplanting
experienced teams of bacteria, including all possible good and true
gut bacteria, from the guts of healthy donors to those with
Clostridium difficile infections. Luckily, such a transplant is relatively
easy to carry out (it has been used for decades by veterinary
practitioners to cure many diseases). All you need are some healthy
feces, complete with bacteria, and that’s it. The treatment is known
as fecal bacteriotherapy, or more directly, a fecal transplant. The
feces used in medical fecal transplants are not pure, but they are
purified. Then, it does not really matter whether they enter through
the front or back door, so to speak.
Almost all studies show a success rate of around 90 percent in
treating previously incurable diarrhea caused by Clostridium difficile.
Few medical drugs have such a high success rate. Despite these
positive results, the treatment can currently be used only on patients
with truly hopeless cases of incurable diarrhea. The danger is that
other diseases or potentially harmful bacteria might be transplanted
along with the donor stool. Some companies are already working to
develop artificial stool that they can guarantee is free of any harmful
elements. If they succeed, the therapy is likely to become much
more widespread.
Probiotics’ greatest potential probably lies in transplanting
beneficial bacteria to the gut, where they would settle permanently
and grow. Such transplants have already helped patients with severe
diabetes. Scientists are currently investigating whether they can also
be used to prevent patients from ever developing full-blown type 1
diabetes.
The connection between stool and diabetes may not be
immediately obvious to everyone. But, in fact, it is not as absurd as it
seems. It is not just defensive bacteria that are transplanted with the
stool, but an entire microbial organ that plays an important part in
regulating the body’s metabolism and immune system. We are still
completely ignorant of more than 60 percent of these gut bacteria.
Looking for species that may have probiotic effects is timeconsuming and difficult, just as the search for medicinal plants was in
the past. Only this time, the search is going on inside us. Every day
we live and every meal we eat influence the great microbial organ
inside us—for better or for worse.
Prebiotics
surrounding the use of prebiotics is to support our
good bacteria by eating certain foods. Prebiotics are much more
suitable for daily use than probiotics. To gain the benefits they offer,
just one condition must be met: good bacteria must already be
present in the gut. These can then be encouraged by eating prebiotic
food, which gives the good bacteria more power over any bad
bacteria that may also be present.
Since bacteria are so much smaller than we are, they view food
from a very different perspective from our own. Every little grain
becomes a major event, a comet of deliciousness. Food we cannot
digest in the small intestine is called dietary fiber or roughage. But,
despite the name, it is not rough on the bacteria of the large
intestine. Quite the opposite, in fact: they love it! Not all kinds, but
some, anyway. Some bacteria love undigested asparagus fibers,
while others prefer undigested meat fibers.
THE CENTRAL IDEA
Some doctors who recommend their patients eat more dietary
fiber do not even really know the reason, which is that they are
prescribing a hearty meal for your bacteria that will benefit you, too.
Finally your gut microbes get enough to eat, so they can produce
vitamins and healthy fatty acids or put the immune system through a
good training session. However, there are always some pathogens
among the bacteria in our gut. They can use certain foodstuffs to
produce substances like indole, phenols, or ammonia. Those are the
substances you find in the chemistry cupboard with a warning
symbol on the bottle.
This is exactly how prebiotics can help: they are roughage that
can only be eaten by nice bacteria. If such a food were available in
the human world, the lunch room at work would be quite an eyeopener! Household sugar is not a prebiotic, for example, because it
is also a favorite of tooth-decay bacteria. Bad bacteria cannot
process prebiotics at all, or hardly, and so they cannot use prebiotics
to produce their evil chemicals. At the same time, good bacteria fed
with prebiotics grow constantly in power and can gain the upper
hand in the gut.
And it is not even very hard to do yourself and your best
microbes a favor with prebiotics. Most people already have a favorite
prebiotic dish that they would not mind eating more often. My granny
always has some potato salad in her fridge, my dad’s specialty is a
great endive salad with mandarin segments (here’s a tip: rinse
endive leaves briefly under warm water—this leaves them crispy but
removes some of the bitterness), and my sister can’t resist
asparagus or black salsify in a creamy sauce.
Artichoke, asparagus, endive, green bananas, Jerusalem artichoke, garlic, onion, parsnips,
black salsify, wheat (wholegrain), rye, oats, leek.
Those are just a few dishes that Bifidobacteria and Lactobacilli
love to eat. We now know that they prefer vegetables from the lily
family (Liliaceae), which includes leeks and asparagus, onions, and
garlic. They also like Compositae plants, which are those from the
sunflower family, including endives, salsify, artichokes, and
Jerusalem artichokes. Resistant starches are also on their list of
favorites.
Resistant starches form, for example, when potatoes or rice are
boiled and then left to cool. This allows the starches to crystalize,
making them more resistant to digestion. This means that more of
your potato salad or cold sushi rice reaches your microbes
untouched. If you don’t already have a favorite prebiotic dish, give
them a try. Eating these dishes regularly has an interesting side
effect—it causes regular cravings for just such foods.
People who eat mainly low-fiber foods like pasta, white bread, or
pizza should not suddenly switch to eating large portions of highfiber foods. That will only overwhelm their underfed bacterial
community. The sudden change will freak the bacteria out, and they
will metabolize everything they can in a fit of euphoria. The result is a
never-ending trumpet concerto from down below. So, the best
strategy is to gradually increase the amount of dietary fiber and not
to feed your bacteria with massive, unmanageable amounts. After
all, the food we eat is still first and foremost for us, and only
secondarily for the inhabitants of our large intestine.
Overproduction of gas is not a pleasant thing—it bloats the gut,
making us feel uncomfortable—but passing a bit of wind is not only
necessary, it is healthy, too. We are living creatures with a miniature
world living inside us, working away and producing many things. Just
as we release exhaust fumes into the Earth’s atmosphere, so must
our microbes, too. It may make a funny sound and it may smell a bit,
but not necessarily. Bifidobacteria and Lactobacilli, for instance, do
not produce any unpleasant odors. People who never need to break
wind are starving their gut bacteria and are not good hosts for their
microbe guests.
Pure prebiotics can be bought at the pharmacy or drugstore.
These include the prebiotic inulin, which is extracted from endives,
and GOS (galacto-oligosaccharides), which are isolated from milk.
These substances have been tested for their health-giving effects
and are pretty efficient at feeding only certain Bifidobacteria and
Lactobacilli.
Prebiotics are nowhere near as well researched as probiotics,
although there are already some sound results pertaining to how
they work. Prebiotics promote good bacteria, resulting in a reduction
in the amount of toxins produced in the gut. People with liver
problems, especially, are unable to detoxify these substances well,
and that can cause serious problems. Bacterial toxins have various
effects on the body, including anything from fatigue and tremors to
comas. When such patients are treated in hospital, they are often
given highly concentrated prebiotics, which usually leads to a
disappearance of their symptoms.
But bacterial toxins also influence Joe Blow with his fully
functioning liver. Toxins can develop, for example, if Joe eats too
little dietary fiber and the fiber is all used up at the beginning of his
large intestine. The bacteria at the end of his gut will then pounce on
any undigested proteins. Bacteria and meat can be a bad
combination—we know it’s never a good idea to eat rotten meat. Too
many meat toxins can damage the large intestine and, in a worstcase scenario, can even cause cancer. The end of the gut is more
prone to cancers on average than the rest of the organ. That’s why
researchers are so keen to test how well prebiotics can protect
against cancer. Early results are promising.
Prebiotics like GOS are interesting because they are also
produced by our own bodies. Ninety percent of the roughage in
human breast milk is GOS, and the remaining 10 percent is made up
of other indigestible fiber. In cow’s milk, GOS accounts for only 10
percent of the fiber content. So it appears there is something about
GOS that is important for human babies. If bottle-fed babies are
given formula milk that contains a little GOS powder, their gut
bacteria looks similar to that of breastfed babies. Some studies
indicate that they are less prone to allergies and neurodermatitis in
later life than other bottle-fed babies. GOS has been approved as an
additive to infant milk formula for a few years, but it is not obligatory.
Since then, interest in GOS has increased, and another of its
effects has now been demonstrated in the laboratory. GOS docks
onto gut cells directly—preferably at locations otherwise favored by
pathogens. That means these prebiotics act as microscopic shields.
Bad bacteria cannot get a good hold and are more likely to slip and
fall away. These results have prompted new studies into GOS as a
way of preventing traveler’s diarrhea.
More research has been carried out into inulin than GOS. Inulin is
sometimes used as a sugar or fat substitute in the food industry
because it is a little bit sweet and has a gel-like consistency. Most
prebiotics are sugars that are linked into chains. When we speak of
sugar, we often mean a particular molecule extracted from sugar
beet or sugar cane, but there are more than a hundred different
kinds of sugar. If, historically, we had developed a sugar industry
based on endive sugar, our sweets would not cause tooth decay.
Sweetness is not in itself unhealthy, we simply eat only the most
unhealthy kind of sweetness.
We are often skeptical about products that are labeled sugar-free
or low fat. Sweeteners like aspartame appear to be carcinogenic,
and other substances used in typical diet products are also used in
factory farming to fatten pigs. So our skepticism is justified. But a
product that contains inulin as a sugar or fat substitute may well be
healthier than one with a full dose of animal fat or sugar. It is worth
reading the label on diet products closely because we can consume
some of them with a clean conscience and our gut microbes will
thank us for it, too.
Inulin cannot bind with our cells as well as GOS. A large and
well-run study in the United Kingdom showed it did not offer any
protection against traveler’s diarrhea, although the test subjects did
report a general improvement in well-being after taking inulin. This
pleasant effect was not reported by members of the control group,
who were given a placebo. Inulin can be produced with different
chain lengths, which is great for attaining a beneficial distribution of
good bacteria. Short inulin chains are eaten by the bacteria at the
start of the large intestine and longer chains are consumed closer to
the end.
The so-called ITFMIX containing chains of differing lengths has
good results, where more surface area equals better results, for
example in the absorption of calcium, which requires bacteria to
pass it through the gut wall. In one experiment, ITFMIX was seen to
improve calcium absorption in young girls by up to 20 percent. That
is good for the bones and can help protect against osteoporosis in
old age.
Calcium is such a good example because it shows the limits of
what can be achieved with prebiotics. Firstly, you have to ingest
enough calcium for an effect to kick in, and secondly, prebiotics can
do nothing if the problem lies with other organs. When many women
go through menopause, their bones get weaker. This is due to a midlife crisis in the ovaries. They have to say goodbye to their life of
producing hormones and learn how to enjoy their retirement. But the
bones miss those hormones! No prebiotic in the world can help with
this kind of osteoporosis.
Nevertheless, we should not underestimate the power of
prebiotics. Almost nothing influences our gut bacteria as much as the
food we eat. Prebiotics are the most powerful tool at our disposal if
we want to support our good bacteria—that is, those that are already
there and are there to stay. Prebiotic creatures of habit, like my
potato salad–addicted granny, are doing the best part of their
microbial organ a favor without even knowing it. Incidentally, her
second favorite vegetable is leeks. Whenever everyone else was ill,
she would be there with a big smile and some soup, merrily playing
us a few songs on the piano. I don’t know if her defenses had
anything to do her microbes, but it’s not an illogical conclusion.
So, we should remember: good bacteria do us good. We should
feed them well so they can populate as much of our large intestine
as possible. Pasta and bread made of white flour on factory
production lines are not enough. We need to include real roughage,
made of real dietary fiber in vegetables and fruit. This roughage can
also satisfy a sweet tooth and taste delicious. It can be fresh
asparagus, sushi rice, or pure, isolated prebiotics from the pharmacy.
Our bacteria will like it, and they will thank us with their good
services.
microscope, bacteria look like nothing but little, bright
spots against a dark background. But taken together, their sum is
much greater than their parts. Each one of us hosts an entire
population. Most sit in our mucus membrane, diligently training our
immune system, soothing our villi, eating what we don’t need, and
producing vitamins for us. Others keep close to the cells of the gut,
needling them or producing toxins. If the good and the bad are in
equilibrium, the bad ones can make us stronger and the good ones
can take care of us and keep us healthy.
SEEN UNDER THE
(PART FOUR)
UPDATE ON
THE BRAIN-GUT
CONNECTION
WHEN I FIRST sat down in 2013 to write about the brain-gut axis, I
spent an entire month staring at a blank screen. At that time, the
brain-gut axis was still an extremely new field of research—nearly all
the studies carried out until then had been on animals, and so the
area was more one of speculation and hypotheses than hard facts. I
was determined to include information about the experiments and
theories that existed; but, at the same time, I was anxious to avoid
raising false hopes or spreading half-truths by jumping the academic
gun, so to speak. As I sat sniffling at my sister’s kitchen table one
gray Thursday, moaning that I wouldn’t be able to come up with a
text that was both accurate and clear enough, she eventually told
me, almost as a command, “Put your head down and just write up
what you understand of it, and if there’s more or better information in
a few years’ time, I’m sure you can add it then.” And that’s exactly
what I’ve done.
New Discoveries
DOING ACADEMIC RESEARCH is like walking through unfamiliar territory
in the fog. There are few people who would wish to do that every
day, happily snapping photos of the new bushes or buildings that
emerge from the mist. Sometimes, you can follow a thread for ages,
only to find that it is your own sweater that is unraveling. And when
that happens, coming home and telling your loved ones what
discoveries you’ve made is not quite so cool.
A couple of years ago, we knew that some depressed mice could
be cheered up by certain bacteria, and we knew of rats whose
character changed completely when other rats’ gut bacteria were
transplanted into their bodies, and thus the term “psychobiotics” was
coined. It describes microbes that have psychological effects—and
which may even be useful in treating conditions like depression. But
those animal studies still left us wondering whether such
psychobiotics could actually affect humans’ mental health.
There are now some twenty reliable studies of this kind involving
human subjects. Three of the bacteria cocktails tested appeared to
have no such effect, but all the rest (and this is the more exciting
piece of news) do influence the human psyche. Overall, a realistic
view of the picture so far is that bacteria don’t cause sudden mood
swings; rather, their effect on our emotional state is gradual, often
not appearing until three to four weeks after the microbes are
administered, and their effect may be fairly limited. Medical thought
has also undergone a development when it comes to stress, and the
gut has been recognized as playing an important role.
What exactly is going on here, and how strong the effects might
be, are still under investigation, with nearly every research team
concentrating on different kinds of bacteria.
Mood
experiments into our mood, a
stimulating initial question is: what emotions constitute our moods?
What are they made up of, so to speak? Most researchers try to
answer this with the aid of questionnaires. The many different kinds
of questions are categorized according to ranges of feelings: from
depressive to cheerful, from fearful to self-assured, from quicktempered to sweet-tempered, from being concerned (for example,
about personal physical well-being) to being positive, and so on.
And that is how a group of English researchers began their first,
tentative trials. Lactobacillus casei Shirota (a bacterium you may
know from the yogurt drinks available at most supermarkets)
improved the disposition of the most ill-tempered third of their test
subjects after they had taken it for only three weeks, from
“depressive” toward “cheerful.” The subjects with a better general
mood saw no further improvement in their spirits, and other feelings,
such as anger or anxiety, were not affected to any significant degree.
That was not the case for a study carried out in France. Scientists
wanted to investigate a combination of two types of bacteria
(Bifidobacterium longum and Lactobacillus helveticus, which are
often found in their abbreviated forms, B. longum and L. helveticus,
in lists of ingredients). After four weeks, the test subjects
experienced a positive improvement not only in their depressive
tendencies, but also in parameters such as anger; or, for example,
FOR RESEARCHERS CONDUCTING
they showed a propensity to perceive their own physical aches and
pains as less severe.
A Dutch team took a more specific approach to the category of
mood itself. They were particularly interested in a certain kind of
mood: those minor, recurrent, routine lows familiar to everybody,
even those of a perfectly healthy mental constitution. Nothing terrible
has happened, and we really can’t even pinpoint what’s causing our
bad mood—we just feel less perky than usual. Such moments of
gloom rarely warrant a mention in our day-to-day conversations or in
the media—but they are currently a hot topic among research
psychologists. What the researchers are interested in is not the
blues themselves, but how we react to them.
This is among the most accurate indicators of whether a healthy
person might develop depression or not. Above all, studies have
repeatedly shown that the least favorable reaction is fretful brooding
—about who might be to blame for our woes, for example.
In this study, the test subjects were asked to spend several
minutes imagining themselves in the following situation. It’s definitely
not your day today, you don’t feel in top form, but nothing serious has
happened to put you in this mood. The subjects then evaluated their
own reaction to this mood, according to statements such as the
following.
“When I feel that way, I have much less patience and I lose my
temper more quickly.”
“When I feel that way, I brood a lot over everything that’s wrong
with my life at the moment, or about what my life might have been
like if it had taken a different turn.”
Or, “When I’m down, I feel that everything is hopeless.”
In the fine old tradition of test questionnaires, the subjects were
given the following five options to rate on a scale of 0 to 4: Nope,
never really / Rarely / Sometimes / Often / Oh yes — absolutely!
Before they began taking the bacteria, the test subjects’ average
scores were about 43 out of a total of 136 points. Thus, they were
within the healthy average range and did not display any brooding,
angry, or despairing tendencies. They then took the bacteria mixture
every day for four weeks. Mouth open, powder in, swallow it down.
The group that were given a placebo (without their knowledge)
barely changed their responses at all. But those who took the real
bacteria improved their scores—in particular, in two areas, anger and
brooding—by about 10 percent at least (which means roughly half
the questions in those areas were answered one degree more
positively).
This is not the same effect as would have been achieved if they
had been given cocaine—or a powerful tranquilizer—but it is also not
the same effect as that of the placebo. Results like these lead us to
the question of how great the gut’s influence on our mood is. They
also raise the question of what aspects of our mood it can affect.
Stress
be seen as originating in various parts of our nervous
system, stress is better described as the state the nervous system is
in. A stressed nervous system is like a taut bowstring—in a constant
state of alertness and sensitive to any external stimulus. Such a
state is excellent for tackling an obstacle course or reacting to a
dangerous situation while driving. However, as a permanent
condition, such a state is pretty costly. . . comparable to taking a
monster truck to drive to the supermarket around the corner. The gut
lends the brain a large amount of energy in order to deal with the
stress (see page 133). Could our guts also help relieve feelings of
stress? As a way of helping themselves, so to speak?
WHILE MOOD CAN
In this field, the wait for newer results has been worth it, as the
research has changed tack. The initial conclusion following the first
experiments with human subjects was that a stressful daily routine or
a scary exam was always equally stressful or frightening for
subjects, no matter which lovely bacteria they fed to their guts.
However, it was concluded, microbes could help reduce the physical
effects of stress, such as stress hormone levels, nervous stomach
aches, nausea, diarrhea, and susceptibility to colds.
However, a closer examination of those studies reveals an
interesting indication. One species of bacteria also altered people’s
subjective level of stress—although this appeared to be the case
only in one subgroup of subjects: the sleep-deprived ones. Those
who slept less in the run-up to an exam were always more stressed.
This effect was less pronounced among subjects who swallowed a
daily dose of Bifidobacterium bifidum. They were still stressed—but a
little less so than their peers who slept equally badly but did not get
the bacterium.
In this study, 581 subjects were divided into four groups a couple
of weeks before the study began. One group received capsules
containing a powder with no bacteria; the other three groups were
each given a different type of bacteria: Bifidobacterium bifidum,
Lactobacillus helveticus, and Bifidobacterium infantis. Lactobacillus
helveticus and Bifidobacterium infantis, however, did not show the
same effect as Bifidobacterium bifidum.
The result with Bifidobacterium bifidum encouraged scientists to
investigate the microbial world in more depth—after all, a bacterium
had now been found that managed something no other bacterium
had been shown to do: reduce feelings of stress. It was not long
before new results emerged from Ireland. Some researchers—those
who had also carried out the experiment with the swimming mice
(see page 126)—now ventured into the arena of human trials. One
particular Bifidobacterium (Bifidobacterium longum 1714) had shown
itself to be highly effective in their experiments with mice. It reduced
stress parameters and improved the lab animals’ memory. So the
Irish scientists tested it on a small group of human animals.
The participants in this study were asked to fill out an online
questionnaire about their feelings of stress every day. They were
also called into the lab three times within a period of eight weeks, in
order to do the following:
1. Put on a funny helmet.
2. Plunge one of their hands into ice-cold water.
3. Solve mental puzzles on a tablet PC.
THE FUNCTION OF the funny helmet was to measure the activity
levels in various parts of the subjects’ brains. If you were to make
your beloved wear this helmet while you were telling him or her
about your boring day at the office, you would be able to watch as
the level of activity in the listening area of their brain slowly declined
and the day-dreaming regions revved up for a party.
Plunging subjects’ hands into unbearably cold water is a triedand-true method of assessing their stress levels. A measurement is
taken of the amount of time subjects are able to keep their hands in
the icy water, while swabbing their mouths regularly with cotton
buds. The cotton buds absorb saliva, which can be analyzed to
measure the amount of stress hormones it contains. No matter how
often the test is repeated, the subjects’ reactions are always the
same. A nervous system that signals stress due to cold is not a
creature of habit—it does not get less sensitive over time when
exposed to low temperatures repeatedly or for a long period of time.
If it did, we would perceive the weather as getting increasingly
warmer as winter progressed.
As soon as the test subjects had had enough and rescued their
hands from their freezing fate, they were asked a number of
questions. The researchers wanted to know how anxious they felt
immediately after experiencing a rush of excited hormones.
Almost every parameter was different in some way after a fourweek course of Bifidobacteria. In the online questionnaires, the test
subjects reported around 15 percent lower levels of day-to-day
stress, as compared with the subjects who received a placebo. The
cold-water, hand-immersion test still triggered the same reaction (as
expected—after all, the water was still freezing cold), but with an
overall stress hormone level that was lower than before.
Furthermore, those hormones did not lead to increased anxiety.
The electrode helmet and tablet-based teasers were also not
simply for the researchers’ amusement. The “bacteria group” made
around two to five fewer mistakes in the memory tasks, compared
with the placebo group (who made one to three fewer mistakes)—
already a successful result. This effect was also made visible by the
helmet. One area of the brain that we use for learning, and which
becomes weaker in patients with Alzheimer’s, now showed
increased activity. The placebo had no such effect—but with the
bacteria, it was clear.
Our gut can send impulses to the brain—for example, via nerve
fibers (see page 126). The Irish research team came up with another
possible explanation—bacteria could have improved memory
function by reducing the subjects’ stress-hormone levels. That might
work like this: the brain structure that stores our memories and links
them to each other (the hippocampus) is very densely populated with
sensors that detect stress hormones. If the hippocampus registers
large amounts of such hormones, the brain cuts back the level of
activity there. After all, if you are running away from a wild animal,
you don’t need to waste energy remembering which plants you pass
by. During stressful times in our lives, we develop a kind of tunnel
vision—to enable us to direct our attention to the problem at hand.
This observation is interesting—not only for fans of
Bifidobacterium longum 1714, but also for patients with gut
conditions who find it difficult to concentrate as well as usual during a
flare-up, and for school students, for example, who have trouble
cooperating with their brains during a tough test. In the end, it may
not really matter whether the state of stress is reported by the gut or
the brain. Both organs are able to use the nervous system and
messenger substances in the blood to stimulate the adrenal gland
(the organ that eventually produces stress hormones). And this is
precisely where we may return to the issue of mood.
Let’s go back to those little, day-to-day downers studied by the
group of Dutch scientists. Remember—no matter how nice our lives
may be, we all have them from time to time. Those who tend to react
to such a mood by brooding over their problems will find that our
modern world offers a rich palette of problems to ponder. Even more
importantly, these are often problems we can do nothing about.
Some politician somewhere in the world says something stupid, but
in the past hardly anyone would have got wind of it. Elsewhere, a
plane comes down, killing an entire football team you would never
otherwise have heard about. Someone or other puts a picture of her
perfect life online, and we end up comparing ourselves unfavorably
to something we would never have seen in the past.
If we engage in it enough, brooding over problems that cannot be
changed can result in feelings of stress. The resultant stress
hormones serve to increase that tunnel vision. And it becomes
increasingly difficult for us to see anything beyond our own problems.
And this, in turn, further increases our level of stress. Voilà: we have
a vicious circle. A physiological system that was meant to help us in
times of stress is thus co-opted, and we increasingly slide into a
behavior pattern of “stressed griping,” rather than directly observing
the world around us, asking inquisitive questions, or taking care of
our well-being.
Depression
of research indicates that our gut has about a 10to 15-percent influence on feelings of melancholy, anger, or stress. It
tells the brain what is happening inside us, and that information may
be worrying or reassuring. So it could be partly responsible when we
slide into a certain mood. However, this says nothing about the
extent of the gut’s involvement in the process of emerging from a
period of fully fledged depression.
Preliminary experiments aimed at answering this question give
cause for optimism. A group of Irish researchers, for example,
harvested gut bacteria from people with depression and implanted
them in rats. This is not the kind of microbial exchange that happens
when you shake hands with someone: the scientists first removed all
other microbes from the rats’ intestinal system and then
administered highly concentrated doses of the harvested bacteria.
The rats developed depressive behaviors that they had not displayed
previously.
When it comes to purely human experiments, research is still at a
very early stage. A common tool in such research is the Becks
Depression Inventory psychometric test. This test helps scientists
determine the severity of a patient’s depression (and, for example,
whether they are dealing with a case of clinical depression or a
temporary bout of the blues). Perhaps surprisingly, the list of twentyone questions does not only ask respondents whether they feel sad
or dissatisfied; it also includes questions about problems with
sleeping, difficulty making decisions, increasing health worries, or a
noticeable lack of interest in sex (compared with the past). Basically,
these are indirect questions about the various hormone systems in
our body.
THE CURRENT STATE
So far, there are only two studies that have investigated, under
controlled conditions, the effect of probiotic bacteria on depression.
The first study, in 2015, found that a combination of two kinds of
bacteria (Lactobacillus acidophilus and Bifidobacterium bifidum) and
medication improved patients’ condition, but the effect was slight
once all possible interference factors were removed from the
calculations. And a study in 2017 found that two types of bacteria
(Lactobacillus helveticus and Bifidobacterium longum) had no
influence on depression. However, the researchers did find an
indication that a patient’s vitamin D level may influence this effect. In
test subjects with sufficiently high levels of vitamin D in their blood,
the microbes appeared to improve their mood; however, the overall
number of subjects was too small to allow a scientific conclusion
from this study.
These are the first two steps on a new journey in research. If we
continue down this path, we will eventually see which way it is
leading us. Could we perhaps use the gut to prevent depression
before it occurs? Are bacteria better suited as a complementary
treatment, to be used alongside medication, therapy, and lifestyle
changes? Or should treatments for depression perhaps target
multiple possible causes at once—that is, the gut (via bacteria and
diet), the brain (with drugs and therapy), and other possible causes
(such as vitamin levels, physical activity, or working conditions)? It
may also be the case that there are many different kinds of
depression—some for which the influence of the gut is greater and
therefore more important in their treatment, and others for which this
is not the case.
The goal of this journey should not be to discover some kind of
super-bug, which we would all take a daily dose of. The aim is also
not to produce a population of permanently happy people. Rather,
the aim should be to reach a better understanding of our bodies and
how we live in them. This includes being aware of what is going on
inside our bodies, rather than looking only for external causes of
stress or mood swings. If we were to discover particularly effective
microbes to support us along the way, that would be an excellent
thing. But while scientists are still searching through the fog, we
should learn to appreciate what we already have: good microbes
inside us and around us, and ancient knowledge, to which we should
pay much more heed.
Clever Cravings for Fermented Foods
SOMETIMES IT IS not necessary to understand our desires and
cravings. If a person occasionally enjoys rolling around on their
living-room floor for no apparent reason, let them. However, it can
sometimes be both useful and interesting to find out why we develop
the desire to eat and drink what we do.
Take a glass of water and add an equal amount of sugar to that
contained in the same volume of cola. Few people would want to
drink the resulting mixture. And if we did, we would probably feel
disgust at the idea of downing a second glass. This is because our
bodies are cleverer than we think.
If we now do something that several million years of evolution
has not been able to prepare us for, the experiment ends with a very
different result. If we add a little citric acid to the sugar water
(represented by carbonic and phosphoric acid in cola)—hey presto!
We have a delicious drink. We down the glass in one gulp, and our
brain claps its hands in delight: hooray!
Our bodies are familiar with acid, from fruit and good bacteria (for
example, the lactic acid bacteria in yogurt). When the acid is not too
strong and comes in combination with other nutrients, it gains the
trust of our taste buds. Thus we like to include an acid component
when we cook a pleasant-tasting meal—tomatoes in the sauce, a
squeeze of lemon over the fish, a glug of wine over the frying onions.
This well-placed pleasure is fascinating for anyone with an interest in
microbes. A pertinent question might be: when we fancy a sour
ingredient in our meal, are we really craving good bacteria?
Down the millennia of history, anyone with a yen for a taste of
sour would satisfy their hunger with good microbes. Our forebears
fermented cabbage to create sauerkraut and drank wine rather than
water (which was usually too contaminated to drink untreated in the
Middle Ages). They still baked their bread using real sourdough, and
made their own sour milk and yogurt products. They did not have
access to citrus fruits or acidified carbonated drinks. This
observation gives cause for a little experiment you can carry out for
yourself.
Fermenting Vegetables
with Bacteria at
Home—AKA Making
Sauerkraut
bacteria to pre-digest your food. Bad
bacteria and molds do not ferment your food nicely, but spoil it and
render it inedible. Good bacteria, however, process our food to make
it easier for us to digest. They are better than our digestive enzymes
at splitting open cabbage cells (or other plant cells). In this way, they
make the work of the gut much easier and even produce additional
vitamins in the process. They also produce acids that kill off any
dangerous bacteria, thus preserving the food for longer. Since good
bacteria are everywhere, just hanging around in the environment, it
makes sense to provide them with a useful job to do and something
to eat. This helps them multiply and gain more power.
FERMENTING MEANS GETTING
1. Cabbage is the classic, but almost any vegetable that can be
eaten raw can also be fermented. Carrots and gherkins, for
example (gherkins are the pinnacle of pickling, however, as
precise procedures must be followed if they are to remain crisp to
the bite). Some good bacteria will already be on the cabbage
leaves or the skin of the carrots, so there is no need to add any
particular bacteria to them. This is why it can be beneficial to buy
vegetables that have not been treated with pesticides, etc.
2. Depending on how long you want the fermentation process to
take, slice your vegetables thinly or grate them (= one week’s
fermentation time) or leave them whole (= four to six weeks’
fermentation time). You need to make sure you avoid
contamination as you work. You don’t want just any old kitchen
bacteria joining your product in the jar.
3. Add one-third of an ounce to half an ounce (10 to 15 grams) of
salt for every 2.2 pounds (1 kilogram) of vegetables. This slows
the growth of bacteria in general, preventing bad germs from
commandeering the process before the good ones can do their
work. It is important to add the correct amount of salt: too much
will prevent the fermentation process altogether; too little can
result in the food going off and tasting bad. Sea salt is a good
choice, but do not use iodized salt under any circumstances as
the iodine inhibits the bacteria’s growth too much.
4. Knead the mixture with appropriate fervor. This is to thoroughly
mix the salt into the concoction and to help partially break down
particularly tough cell walls. The salt helps extract the water from
the cabbage cells, which can be used later as the pickling liquid.
5. Press the cabbage firmly into a jar with an airtight seal. It is
important to make sure that all the vegetable matter is submerged
beneath the liquid so that it is not exposed to oxygen, which
disturbs the fermenting bacteria. Any parts that stick out above
the liquid will not be protected by the acid and could go moldy. If
your cabbage or carrots have not produced enough liquid of their
own to cover them completely, you can add more salted water.
Add a generous teaspoon of salt for every 0.85 ounces (250 ml)
of water. If there is still some vegetable matter sticking out above
the surface of the liquid, you can add a weight to press it down.
(Special “sauerkraut weights” are available, in Germany, at least!
—but a rock or stone of the right size that has been cleaned by
boiling it in water will do the job just as well.) Those who prefer a
particular flavor to their sauerkraut can now add almost anything
they want to the jar, such as caraway seeds, beetroot, or,
particularly good with carrots, a little ginger.
YOU MAY SOMETIMES see little bubbles of gas rising through the
liquid as the fermentation process progresses. This is why people in
ancient cultures, who had no knowledge of the microbial world,
would sometimes dance around the fermentation vats, as they
thought this would encourage the vegetables to bubble. Others, by
contrast, would afford the barrels calm so as not to disturb the gods
in their work. Once fermentation is complete and everything is ready,
the result should taste sour, and should not be slimy in consistency
or taste too strongly of alcohol. From this stage, it can be kept in the
fridge.
Incidentally, it is at this stage that the sauerkraut you buy from the
supermarket is boiled to pasteurize it. This not only kills off the
bacteria, but it also destroys some of the vitamin C they have
produced. Manufacturers therefore often add vitamin C powder after
pasteurization. The acid it relies on means that fermentation is the
safest way to preserve food—canned or bottled foods have been
known to cause illness due to temperature-resistant bacteria, but no
case of illness caused by fermented foods has ever been reported.
You can now add a spoon or two of your homemade sauerkraut
or sour carrots to just about any meal: in salad instead of vinegar, on
a burger instead of gherkin pickled in vinegar, in soups and stews
(add just before serving), with vegetable or rice dishes, or, for those
feeling particularly adventurous, with some honey in your breakfast
porridge. Then just wait and see if you start craving this special
“sourness” more and more. When your appetite decides it likes
something after trying it once or twice—you might as well go with it.
Acknowledgments
THIS BOOK WOULD not exist if it weren’t for my sister, Jill. Without your
free, rational, and inquisitive mind, I would have been stuck many
times in a world where obedience and conformity are easier than
courage and the will to make necessary mistakes. Although you lead
a busy life yourself, you were always there, ready to go through my
texts with me and inspire me with new ideas. You taught me how to
work creatively. Whenever I feel bad, I remember we are made of the
same stuff and each of us uses her talents differently. I would like to
thank Ambrosius, who shielded me from too much work with a
protective arm. I would also like to thank my family and my godfather
for surrounding me like a forest surrounds a tree, keeping me rooted
even when strong winds are blowing. I also thank Ji-Won for keeping
me nourished so often during the writing of this book—with food and
her wonderful nature. My thanks go to Anne-Claire and Anne for
their help with even the trickiest of questions!
I thank Michaela and Bettina, without whose sharp minds the
writing of this book would never have come about. If it weren’t for my
medical studies I would never have had the knowledge necessary to
write this book, so I thank all my good teachers and professors, as
well as the German state, which pays for my university studies. To
everyone who has contributed their hard work to the realization of
this book—from press officers, publishers, manufacturers, printers,
marketers, proofreaders, booksellers, postal workers, to those of you
reading this now: Thank you!
References
contains references to sources dealing with content
not normally covered in the standard text books.
THIS LIST MAINLY
Part One
BANDANI, A.R.: “EFFECT of Plant a-Amylase Inhibitors on Sunn Pest, Eurygaster
Integriceps Puton (Hemiptera: Scutelleridae), Alpha-Amylase Activity.” In: Commun Agric
Appl Biol Sci. 2005; 70 (4): pp. 869–873.
Baugh, R.F. et al.: “Clinical Practice Guideline: Tonsillectomy in Children.” In: Otolaryngol
Head Neck Surg. 2011 January; 144 (Suppl. 1): pp. 1–30.
Bengmark, S.: “Integrative Medicine and Human Health—The Role of Pre-, Pro- and
Synbiotics.” In: Clin Transl Med. 2012 May 28; 1 (1): p. 6.
Bernardo, D et al.: “Is Gliadin Really Safe for Non-Coeliac Individuals? Production of
Interleukin 15 in Biopsy Culture from Non-Coeliac Individuals Challenged with Gliadin
Peptides.” In: Gut. 2007 June; 56 (6): p. 889 f.
Bodinier, M. et al.: “Intestinal Translocation Capabilities of Wheat Allergens Using the Caco2 Cell Line.” In: J Agric Food Chem. 2007 May 30; 55 (11): pp. 4576–4583.
Bollinger, R. et al.: “Biofilms in the Large Bowel Suggest an Apparent Function of the
Human Vermiform Appendix.” In: J Theor Biol. 2007 December 21; 249 (4): pp. 826–
831.
Catassi, C. et al.: “Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related
Disorders.” In: Nutrients. 2013 September 26; 5 (10): pp. 3839–3853.
Kim, B.H.; Gadd, G.M.: Bacterial Physiology and Metabolism. Cambridge: Cambridge
University Press, 2008.
Klausner, A.G. et al.: “Behavioral Modification of Colonic Function. Can Constipation Be
Learned?” In: Dig Dis Sci. 1990 October; 35 (10): pp. 1271–1275.
LAMERS, K.L. et al.: “Gliadin Induces an Increase in Intestinal Permeability and Zonulin
Release by Binding to the Chemokine Receptor CXCR3.” In: Gastroenterology. 2008
July; 135 (1): pp. 194–204.
LEDOCHOWSKI, M. ET al.: “Fructose- and Sorbitol-Reduced Diet Improves Mood and
Gastrointestinal Disturbances in Fructose Malabsorbers.” In: Scand J Gastroenterol.
2000 October; 35 (10): pp. 1048–1052.
LEWIS, S.J.; HEATON, K.W.: “Stool Form Scale as a Useful Guide to Intestinal Transit
Time.” In: Scand J Gastroenterol. 1997 September; 32 (9): pp. 920–924.
MARTÍN-PELÁEZ, S. ET al.: “Health Effects of Olive Oil Polyphenols: Recent Advances and
Possibilities for the Use of Health Claims.” In: Mol. Nutr. Food Res. 2013; 57 (5): pp.
760–771.
PAUL, S.: Paläopower—Das Wissen der Evolution nutzen für Ernährung, Gesundheit und
Genuss. Munich: C.H. Beck-Verlag, 2013 (2nd Edition). (In German)
SIKIROV, D.: “ETIOLOGY and Pathogenesis of Diverticulosis Coli: A New Approach.” In:
Med Hypotheses. 1988 May: 26 (1): pp. 17–20.
SIKIROV, D.: “COMPARISON of Straining during Defecation in Three Positions: Results and
Implications for Human Health.” In: Dig Dis Sci. 2003 July; 48 (7): pp. 1201–1205.
THORLEIFSDOTTIR, R.H. et al.: “Improvement of Psoriasis after Tonsillectomy Is
Associated with a Decrease in the Frequency of Circulating T Cells That Recognize
Streptococcal Determinants and Homologous Skin Determinants.” In: J Immunol. 2012;
188 (10): pp. 5160–5165.
VAREA, V. et al.: “Malabsorption of Carbohydrates and Depression in Children and
Adolescents.” In: J Pediatr Gastroenterol Nutr. 2005 May; 40 (5): pp. 561–565.
WISNER, A. et al.: “Human Opiorphin, a Natural Antinociceptive Modulator of OpioidDependent Pathways.” In: Proc Natl Acad Sci USA. 2006 November 21; 103 (47): pp.
17979–17984.
Part Two
AGUILERA, M. ET al.: “Stress and Antibiotics Alter Luminal and Wall-Adhered Microbiota
and Enhance the Local Expression of Visceral Sensory-Related Systems in Mice.” In:
Neurogastroenterol Motil. 2013 August; 25 (8): pp. e515–e529.
BERCIK, P. ET al.: “The Intestinal Microbiota Affect Central Levels of Brain-Derived
Neurotropic Factor and Behavior in Mice.” In: Gastroenterology. 2011 August; 141 (2):
pp. 599–609.
BRAVO, J.A. ET al.: “Ingestion of Lactobacillus Strain Regulates Emotional Behavior and
Central GABA Receptor Expression in a Mouse via the Vagus Nerve.” In: Proc Natl Acad
Sci USA. 2011 September 20; 108 (38): pp. 16050–16055.
BUBENZER, R.H.; KADEN, M.: at www.sodbrennen-welt.de (retrieved October 2013).
CASTRÉN, E.: “NEURONAL Network Plasticity and Recovery from Depression.” In: JAMA
Psychiatry. 2013: 70 (9): pp. 983–989.
CRAIG, A.D.: “How Do You Feel—Now? The Anterior Insula and Human Awareness.” In:
Nat Rev Neurosci. 2009 January; 10 (1): pp. 58–70.
ENCK, P. ET al.: “Therapy Options in Irritable Bowel Syndrome.” In: Eur J Gastroenterol
Hepatol. 2010 December; 22 (12): pp. 1402–1411.
FURNESS, J.B. ET al.: “The Intestine as a Sensory Organ: Neural, Endocrine, and Immune
Responses.” In: Am J Physiol Gastrointest Liver Physiol. 1999; 227 (5): pp. G922–G928.
HUERTA-FRANCO, M.R. ET al.: “Effect of Psychological Stress on Gastric Motility
Assessed by Electrical Bio-Impedance.” In: World J Gastroenterol. 2012 September 28;
18 (36): pp. 5027–5033.
KELL, C.A. ET al.: “The Sensory Cortical Representation of the Human Penis: Revisiting
Somatotopy in the Male Homunculus.” In: J Neurosci. 2005 June 22; 25 (25): pp. 5984–
5987.
KELLER, J. ET al.: “S3-Leitline der Deutschen Gesellschaft für Verdauungs-und
Stoffwechselkrankheiten (DGVS) und der Deutschen Gesellschaft für
Neurogastroenterologie und Motilität (DGNM) zu Definition, Pathophysiologie,
Diagnostik und Therapie intestinaler Motilitätsstörungen” [S3 Guidelines of the German
Society for Digestive and Metabolic Diseases (DGVS) and the German Society for
Neurogastroenterology and Motility (DGNM) for the Definition, Pathophysiology,
Diagnosis, and Treatment of Intestinal Motility Disorders]. In: Z Gastroenterol. 2011; 49:
pp. 374–390. (In German)
KEYWOOD, C. ET al.: “A Proof of Concept Study Evaluating the Effect of ADX10059, a
Metabotropic Glutamate Receptor-5 Negative Allosteric Modulator, on Acid Exposure
and Symptoms in Gastro-Oesophageal Reflux Disease.” In: Gut. 2009 September; 58
(9): pp. 1192–1199.
KRAMER, H. ET al.: “Tabuthema Obstipation: Welche Rolle spielen Lebensgewohnheiten,
Ernährung, Prä- und Probiotika sowie Laxanzien?” [Taboo Subject Constipation: What
Part Do Habits, Diet, Pre- and Probiotics, and Laxatives Play?]. In: Aktuelle
Ernährungsmedizin. 2009; 34 (1): pp. 38–46. (In German)
LAYER, P. ET al.: “S3-Leitlinie Reizdarmsyndrom: Definition, Pathophysiologie, Diagnostik
und Therapie. Gemeinsame Leitlinie der Deutschen Gesellschaft für Verdauungs- und
Stoffwechselkrankheiten (DGVS) und der Deutschen Gesellschaft für
Neurogastroenterologie und Motilität (DGNM)” [S3 Guideline on Irritable Bowel
Syndrom: Joint Guideline of the German Society for Digestive and Metabolic Diseases
(DGVS) and the German Society for Neurogastroenterology and Motility (DGNM)]. In: Z
Gastroenterol. 2011; 49: pp. 237–293. (In German)
MA, X. et al.: “Lactobacillus Reuteri Ingestion Prevents Hyperexcitability of Colonic DRG
Neurons Induced by Noxious Stimuli.” In: Am J Physiol Gastrointest Liver Physiol. 2009
April; 296 (4): pp. G868–G875.
MAYER, E.A.: “GUT Feelings: The Emerging Biology of Gut-Brain Communication.” In: Nat
Rev Neurosci. 2011 July 13; 12 (8): pp. 453–466.
MAYER, E.A. ET al.: “Brain Imaging Approaches to the Study of Functional GI Disorders: A
Rome Working Team Report.” In: Neurogastroenterol Motil. 2009 June; 21 (6): pp. 579–
596.
MOSER, G. (Ed.): Psychosomatik in der Gastroenterologie und Hepatologie
[Psychosomatics in Gastroenterology and Hepatology]. Vienna; New York: Springer,
2007. (In German)
NALIBOFF, B.D. ET al.: “Evidence for Two Distinct Perceptual Alterations in Irritable Bowel
Syndrom.” In: Gut. 1997 October; 41 (4): pp. 505–512.
PALATTY, P.L. ET al.: “Ginger in the Prevention of Nausea and Vomiting: A Review.” In: Crit
Rev Food Sci Nutr. 2013; 53 (7): pp. 659–669.
REVEILLER, M. ET al.: “Bile Exposure Inhibits Expression of Squamous Differentiation
Genes in Human Esophageal Epithelial Cells.” In: Ann Surg. 2012 June; 255 (6): pp.
1113–1120.
REVENSTORF, D.: Expertise zur wissenschaftlichen Evidenz der Hypnotherapie [Expert
Opinion on the Scientific Evidence for Hypnotherapy]. Tübingen, 2003; at
http://www.meg.tuebingen.de/downloads/Expertise.pdf (retrieved October 2013). (In
German)
SIMONS, C.C. ET al.: “Bowel Movement and Constipation Frequencies and the Risk of
Colorectal Cancer among Men in the Netherlands Cohort Study on Diet and Cancer.” In:
Am J Epidemiol. 2010 December 15; 172 (12): pp. 1404–1414.
STREITBERGER, K. ET al.: “Acupuncture Compared to Placebo-Acupuncture for
Postoperative Nausea and Vomiting Prophylaxis: A Randomised Placebo-Controlled
Patient and Observer Blind Trial.” In: Anaesthesia. 2004 February; 59 (2): pp. 142–149.
TILLISCH, K. ET al.: “Consumption of Fermented Milk Product with Probiotic Modulates
Brain Activity.” In: Gastroenterology. 2013 June; 144 (7): pp. 1394–1401.
Part Three
AGGARWAL, J. ET al.: “Probiotics and their Effects on Metabolic Diseases: An Update.” In:
J Clin Diagn Res. 2013 January; 7 (1): pp. 173–177.
ARNOLD, I.C. ET al.: “Helicobacter pylori Infection Prevents Allergic Asthma in Mouse
Models through the Induction of Regulatory T Cells.” In: J Clin Invest. 2011 August; 121
(8): pp. 3088–3093.
Arumugam, M. ET al.: “Enterotypes of the Human Gut Microbiome.” In: Nature. 2011 May
12; 474 (7353); 1: pp. 174–180.
BÄCKHED, F.: “ADDRESSING the Gut Microbiome and Implications for Obesity.” In:
International Dairy Journal. 2012; 20 (4): pp. 259–261.
BALAKRISHNAN, M.; FLOCH, M.H.: “Prebiotics, Probiotics and Digestive Health.” In: Curr
Opin Clin Nutr Metab Care. 2012 November; 15 (6): pp. 580–585.
BARROS, F.C.: “CESAREAN Section and Risk of Obesity in Childhood, Adolescence, and
Early Adulthood: Evidence from 3 Brazilian Birth Cohorts.” In: Am J Clin Nutr. 2012; 95
(2): pp. 465–470.
BARTOLOMEO, F. Di: “Prebiotics to Fight Diseases: Reality of Fiction?” In: Phytother Res.
2013 October; 27 (10): pp. 1457–1473.
BISCHOFF, S.C.; KÖCHLING, K.: “Pro- und Präbiotika” [Pro- and Prebiotics]. In: Zeitschrift
für Stoffwechselforschung, klinische Ernährung und Diätik. 2012; 37: pp. 287–304.
BORODY, T.J. ET al.: “Fecal Microbiota Transplantation: Indications, Methods, Evidence,
and Future Directions.” In: Curr Gastroenterol Rep. 2013; 15 (8): p. 337.
BRÄUNIG, J.: Verbrauchertipps zu Lebensmittelhygiene, Reinigung und Desinfektion
[Consumer Tips on Food Hygiene, Cleaning and Disinfection]. Berlin: German Federal
Institute for Risk Assessment, 2005. (In German)
BREDE C.: Das Instrument der Sauberkeit. Die Entwicklung der Massenproduktion von
Feinseifen in Deutschland 1850 to 2000 [The Instrument of Cleanliness. The
Development of Fine Soap Mass Production in Germany 1850 to 2000]. Münster et al.:
Waxmann, 2005. (In German)
CAPORASO, J.G. ET al.: “Moving Pictures of the Human Microbiome.” In: Genome Biol.
2011; 12 (5): p. R50.
CARVALHO, B.M.; SAAD, M.J.: “Influence of Gut Microbiota on Subclinical Inflammation
and Insulin Resistance.” In: Mediators Inflamm. 2013; 2013: 986734.
CHARALAMPOPOULOS, D.; RASTALL, R.A.: “Prebiotics in Foods.” In: Current Opinion on
Biotechnology. 2012, 23 (2): pp. 187–191.
CHEN, Y. ET al.: “Association between Helicobacter pylori and Mortality in the NHANES I
Study.” In: Gut. 2013 September; 62 (9): pp. 1262–1269.
DEVARAJ, S. ET al.: “The Human Gut Microbiome and Body Metabolism: Implications for
Obesity and Diabetes.” In: Clin Chem. 2013 April; 59 (4): pp. 617–628.
DOMINGUEZ-BELLO, M.G. ET al.: “Development of the Human Gastrointestinal Microbiota
and Insights from High-Throughput Sequencing.” In: Gastroenterology. 2011 May; 140
(6): pp. 1713–1791.
DOUGLAS, L.C.; SANDERS, M.E.: “Probiotics and Prebiotics in Dietetics Practice.” In: J
Am Diet Assoc. 2008 March; 108 (3): pp. 510–521.
EPPINGER, M. ET al.: “Who Ate Whom? Adaptive Helicobacter Genomic Changes That
Accompanied a Host Jump from Early Humans to Large Felines.” In: PLoS Genet. 2006
July; 2 (7): p. e120.
FAHEY, J.W. ET al.: “Urease from Helicobacter pylori Is Inactivated by Sulforaphane and
Other Isothiocyanates.” In: Biochem Biophys Res Commun. 2013 May 24; 435 (1): pp.
1–7.
FLEGR, J.: “INFLUENCE of Latent Toxoplasma Infection on Human Personality, Physiology
and Morphology: Pros and Cons of the Toxoplasma-Human Model in Studying the
Manipulation Hypothesis.” In: J Exp Biol. 2013 January 1; 216 (Pt. 1): pp. 127–133.
FLEGR, J. et al.: “Increased Incidence of Traffic Accidents in Toxoplasma-Infected Military
Drivers and Protective Effect RhD Molecule Revealed by a Large-Scale Prospective
Cohort Study.” In: BMC Infect Dis. 2009 May 26; 9: p. 72.
FLINT, H.J.: “OBESITY and the Gut Microbiota.” In: J Clin Gastroenterol. 2011 November;
45 (Suppl.): pp. 128–132.
FOUHY, F. ET al.: “High-Throughput Sequencing Reveals the Incomplete, Short-Term
Recovery of Infant Gut Microbiota following Parenteral Antibiotic Treatment with
Ampicillin and Gentamicin.” In: Antimicrob Agents Chemother. 2012 November; 56 (11):
pp. 5811–5820.
FUHRER, A. ET al.: “Milk Sialyllactose Influences Colitis in Mice through Selective Intestinal
Bacterial Colonization.” In: J Exp Med. 2010 December 20; 207 (13): pp. 2843–2854.
GALE, E.A.M.: “A Missing Link in the Hygiene Hypothesis?” In: Diabetologia. 2002; 45 (4):
pp. 588–594.
GANAL, S.C. ET al.: “Priming of Natural Killer Cells by Non-Mucosal Mononuclear
Phagocytes Requires Instructive Signals from the Commensal Microbiota.” In: Immunity.
2012 July 27; 37 (1): pp. 171–186.
GERMAN FEDERAL GOVERNMENT: “Antwort der Bundesregierung auf die Kleine Anfrage
der Abgeordneten Friedrich Ostendorff, Bärbel Höhn, Nicole Maisch, weiterer
Abgeordeter und der Fraktion BÜNDNIS 90/DIE GRÜNEN.” Drucksache 17/10017.
“Daten zur Antibiotikavergabe in Nutztierhaltungen und zum Eintrag von Antibiotika und
multiresistenten Keimen in die Umwelt.” Drucksache 17/10313 [The German Federal
Government’s response to the minor interpellation from members Friedrich Ostendorff,
Bärbel Höhn, Nicole Maisch, other members, and the ALLIANCE 90/THE GREENS
parliamentary group—Parliamentary record 17/10017. Data on the use of antibiotics in
livestock farming and the contamination of the environment by antibiotics and multidrug
resistant bacteria. Parliamentary record 17/10313], 17 July 2012, at
http://dip21.bundestag.de/dip21/btd/17/103/1710313.pdf (retrieved October 2013). (In
German)
GIBNEY, M.J.; BURSTYN, P.G.: “Milk, Serum Cholesterol, and the Maasai—A Hypothesis.”
In: Atherosclerosis. 1980; 35 (3): pp. 339–343.
GLEESON, M. ET al.: “Daily Probiotic’s (Lactobacillus casei Shirota) Reduction of Infection
Incidence in Athletes.” In: Int J Sport Nutr Exerc Metab. 2011 February; 21 (1): pp. 55–
64.
GOLDIN, B.R.; GORBACH, S.L.: “Clinical Indications for Probiotics: An Overview.” In:
Clinical Infectious Diseases. 2008; 46 (Suppl. 2): pp. S96–S100.
GORKIEWICZ, G.: “CONTRIBUTIONS of the Physiological Gut Microflora to Health and
Disease.” In: J Gastroenterol Hepatol Erkr. 2009; 7 (1): pp. 15–18.
GREWE, K.: Prävalenz von Salmonella spp. in der primären Geflügelproduktion und
Broilerschlachtung—Salmonelleneintrag bei Schlachtgeflügel während des
Schlachtprozesses [Prevalence of Salmonella spp. in Primary Poultry Production and
the Slaughter of Broiler Chickens—Salmonella Contamination of Slaughter Poultry
during the Slaughtering Process]. Hanover: Hanover University of Veterinary Medicine,
2011. (In German)
GUSEO. A.: “THE Parkinson Puzzle.” In: Orv Hetil. 2012 December 30; 153 (52): pp. 2060–
2069.
HERBARTH, O. ET al.: “Helicobacter pylori Colonisation and Eczema.” In: Journal of
Epidemiology and Community Health. 2007; 61 (7): pp. 638–640.
HULLAR, M.A.; LAMPE, J.W.: “The Gut Microbiome and Obesity.” In: Nestle Nutr Inst
Workshop Ser. 2012; 73: pp. 67–79.
JERNBERG, C. ET al.: “Long-Term Impacts of Antibiotic Exposure on the Human Intestinal
Microbiota.” In: Microbiology. 2010 November; 156 (Pt. 11): pp. 3216–3223.
JIN, C.; FLAVELL, R.A.: “Innate Sensors of Pathogen and Stress: Linking Inflammation to
Obesity.” In: J Allergy Clin Immunol. 2013 August; 132 (2): pp. 287–294.
JIRILLO, E. ET al.: “Heathy Effects Exerted by Prebiotics, Probiotics, and Symbiotics with
Special Reference to Their Impact on the Immune System.” In: Int J Vitam Nutr Res.
2012 June; 82 (3): pp. 200–208.
JONES, M.L. ET al.: “Cholesterol-Lowering Efficacy of a Microencapsulated Bile Salt
Hydrolase-Active Lactobacillus reuteri NIMB 30242 Yoghurt Formulation in
Hypercholesterolaemic Adults.” In: British Journal of Nutrition. 2012; 107 (10): pp. 1505–
1513.
JUMPERTZ, R. ET al.: “Energy-Balance Studies Reveal Associations between Gut
Microbes, Caloric Load, and Nutrient Absorption in Humans.” In: Am J Clin Nutr. 2011;
94 (1): pp. 58–65.
KATZ, S.E.: The Art of Fermentation: An In-Depth Exploration of Essential Concepts and
Processes from around the World. Chelsea: Chelsea Green Publishing, 2012.
KOUNTOURAS, J. ET al.: “Helicobacter pylori Infection and Parkinson’s Disease: Apoptosis
as an Underlying Common Contributor.” In: Eur J Neurol. 2012 June; 19 (6): p. e56.
KRZNARICA, Z. ET al.: “Gut Microbiota and Obesity.” In: Dig Dis. 2012; 30: p. 196–200.
KUMAR, M. et al.: “Cholesterol-Lowering Probiotics as Potential Biotherapeutics for
Metabolic Diseases.” In: Exp Diabetes Res. 2012; 2012: 902917.
MACFARLANE, G.T. ET al.: “Bacterial Metabolism and Health-Related Effects of
Galactooligosaccharides and Other Prebiotics.” In: J Appl Microbiol. 2008 February; 104
(2): pp. 305–344.
MANN, G.V. ET al.: “Atherosclerosis in the Masai.” In: Am J Epidemiol. 1972; 95 (1): pp.
26–37.
MARSHALL, B. J.: “Unidentified Curved Bacillus on Gastric Epithelium in Active Chronic
Gastritis.” In: Lancet. 1983 June 4; 1 (8336): pp. 1273 ff.
MARTINSON, V.G. ET al.: “A Simple and Distinctive Microbiota Associated with Honey
Bees and Bumble Bees.” In: Mol Ecol. 2011 February; 20 (3): pp. 619–628.
MATAMOROS, S. ET al.: “Development of Intestinal Microbiota in Infants and Its Impact on
Health.” In: Trends Microbiol. 2013 April; 21 (4): pp. 167–173.
MOODLEY, Y. ET al.: “The Peopling of the Pacific from a Bacterial Perspective.” In:
Science. 2009 January 23; 323 (5913): pp. 527–530.
MORI, K. ET al.: “Does the Gut Microbiota Trigger Hashimoto’s Thyroiditis?” In: Discov Med.
2012 November; 14 (78): pp. 321–326.
MUSSO, G. ET al.: “Gut Microbiota as a Regulator of Energy Homeostasis and Ectopic Fat
Deposition: Mechanisms and Implications for Metabolic Disorders.” In: Current Opinion
in Lipidology. 2010; 21 (1): pp. 76–83.
NAGPAL, R. ET al.: “Probiotics, Their Health Benefits and Applications for Developing
Healthier Foods: A Review.” In: FEMS Microbiol Lett. 2012 September; 334 (1): pp. 1–
15.
NAKAMURA, Y.K.; OMAYE, S.T.: “Metabolic Diseases and Pro- and Prebiotics: Mechanistic
Insights.” In: Nutr Metab (Lond). 2012 June 19; 9 (1): p. 60.
NICOLA, J.P. ET al.: “Functional Toll-Like Receptor 4 Conferring Lipopolysaccharide
Responsiveness Is Expressed in Thyroid Cells.” In: Endocrinology. 2009 January; 150
(1): pp. 500–508.
NIELSEN, H.H. ET al.: “Treatment for Helicobacter pylori Infection and Risk of Parkinson’s
Disease in Denmark.” In: Eur J Neurol. 2012 June; 19 (6): pp. 864–869.
NORRIS, V. ET al.: “Bacteria Control Host Appetites.” In: J Bacteriol. 2013 February; 195
(3): pp. 411–416.
OKUSAGA, O.; POSTOLACHE, T.T.: “Toxoplasma gondii, the Immune System, and Suicidal
Behavior.” In: Dwivedi. Y. (Ed.): The Neurological Basis of Suicide. Boca Raton, Florida:
CRC Press, 2012: pp. 159–194.
OTTMAN, N. ET al.: “The Function of Our Microbiota: Who Is Out There and What Do They
Do?” In: Front Cell Infect Microbiol. 2012 August 9; 2: p. 104.
PAVLOVÍC, N. ET al.: “Probiotics-Interactions with Bile Acids and Impact on Cholesterol
Metabolism.” In: Appl Biochem Biotechnol. 2012; 168: pp. 1880–1895.
PETROF, E.O. ET al.: “Stool Substitute Transplant Therapy for the Eradications of
Clostridium difficile Infection ‘RePOOPulating’ the Gut.” In: Microbiome. 2013 January 9;
1 (1): p. 3.
READING, N.C.; KASPER, D.L.: “The Starting Lineup: Key Microbial Players in Intestinal
Immunity and Homeostasis.” In: Front Microbiol. 2011 July 7; 2: p. 148.
ROBERFROID, M. ET al.: “Prebiotic Effects: Metabolic and Health Benefits.” In: Br J Nutr.
2010 August; 104 (Suppl. 2): pp. S1–S63.
SANDERS, M.E. ET al.: “An Update on the Use and Investigation of Probiotics in Health
and Disease.” In: Gut. 2013; 62 (5): pp. 787–796.
SANZA, Y. et al.: “Understanding the Role of Gut Microbes and Probiotics in Obesity: How
Far Are We?” In: Pharmacol Res. 2013 March; 69 (1): pp. 144–155.
SCHMIDT, C.: “THE Startup Bugs.” In: Nat Biotechnol. 2013 April; 31 (4): pp. 279–281.
SCHOLZ-AHRENS, K.E. ET al.: “Prebiotics, Probiotics, and Synbiotics Affect Mineral
Absorption, Bone Mineral Content, and Bone Structure.” In: J Nutr. 2007 March; 137 (3
Suppl. 2): pp. 838S–846S.
SCHWARZ, S. ET al.: “Horizontal versus Familial Transmission of Helicobacter pylori.” In:
PLoS Pathog. 2008 October; 4 (10): p. e1000180.
SHEN, J. ET al.: “The Gut Microbiota, Obesity and Insulin Resistance.” In: Mol Aspects
Med. 2013 February; 34 (1): pp. 39–58.
STARKENMANN, C. ET al.: “Olfactory Perception of Cysteine-S–Conjugates from Fruits
and Vegetables.” In: J Agric Food Chem. 2008 October 22; 56 (20): pp. 9575–9580.
STOWELL, S.R.: “INNATE Immune Lectins Kill Bacteria Expressing Blood Group Antigen.”
In: Nat Med. 2010 March; 16 (3): pp. 295–301.
TÄNGDÉN, T. ET al.: “Foreign Travel Is a Major Risk Factor for Colonization with
Escherichia coli Producing CTX-M–Type Extended-Spectrum ß-Lactamases: A
Prospective Study with Swedish Volunteers.” In: Antimicrob Agents Chemother. 2010
September; 54 (9): pp. 3564–3568.
TEIXEIRA, T.F.: “POTENTIAL Mechanisms for the Emerging Link between Obesity and
Increased Intestinal Permeability.” In: Nutr Res. 2012 September; 32 (9): pp. 637–647.
TORREY, E.F. ET al.: “Antibodies to Toxoplasma gondii in Patients with Schizophrenia: A
Meta-Analysis.” In: Schizophr Bull. 2007 May; 33 (3): pp. 729–736.
TREMAROLI, V.; BÄCKHED, F.: “Functional Interactions between the Gut Microbiota and
Host Metabolism.” In: Nature. 2012 September 13; 489 (7415): pp. 242–249.
TURNBAUGH, P.J.; GORDON, J.L.: “The Core Gut Microbiome, Energy Balance and
Obesity.” In: J Physiol. 2009; 587 (17): pp. 4153–4158.
DE VRESE, M.; Schrezenmeir, J.: “Probiotics, Prebiotics, and Synbtiotics.” In: Adv Biochem
Engin/Biotechnol. 2008; 111: pp. 1–66.
DE VRIESE, J.: “Medical Research. The Promise of Poop.” In: Science. 2013 August 30;
341 (6149): pp. 954–957.
VYAS, U.; RANGANATHAN, N.: “Probiotics, Prebiotics and Synbiotics: Gut and Beyond.” In:
Gastroenterol Res Pract. 2012; 2012: 872716.
WEBSTER, J.P. ET al.: “Effect of Toxoplasma gondii upon Neophobic Behaviour in Wild
Brown Rats, Rattus norvegicus.” In: Parasitology. 1994 July; 109 (pt. 1): pp. 37–43.
WICHMANN-SCHAUER, H.: Verbrauchertipps: Schutz vor Lebensmittelin-fektionen im
Privathaushalt [Tips: Protection against Food Infections in Private Households]. Berlin:
German Federal Institute for Risk Assessment, 2007. (In German)
WU, G.D. ET al.: “Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes.” In:
Science. 2011 October 7; 334 (6052): pp. 105–108.
YATSUNENKO, T. et al.: “Human Gut Microbiome Viewed across Age and Geography.” In:
Nature. 2012 May 9; 486 (7402): pp. 222–227.
ZIPRIS, D.: “THE Interplay between the Gut Microbiota and the Immune System in the
Mechanism of Type 1 Diabetes.” In: Curr Opin Endocrinol Diabetes Obes. 2013 August;
20 (4): pp. 265–270.
Part Four
AKKASHEH, G. ET al.: “Clinical and Metabolic Response to Probiotic Administration in
Patients with Major Depressive Disorder: A Randomized, Double-Blind, PlaceboControlled Trial.” In: Nutrition. 2016; 32: pp. 315–320.
ALLEN, A.P. ET al.: “Bifidobacterium longum 1714 as a Translational Psychobiotic:
Modulation of Stress, Electrophysiology and Neurocognition in Healthy Volunteers.” In:
Transl Psychiatry. 2016; 6, e939; doi:10.1038/tp.2016.191.
BENTON, D. ET al.: “Impact of Consuming a Milk Drink Containing a Probiotic on Mood and
Cognition.” In: Eur J Clin Nutr. 2007; 61: pp. 355–361.
DIOP, L. ET al.: “Probiotic Food Supplement Reduces Stress-Induced Gastrointestinal
Symptoms in Volunteers: A Double-Blind, Placebo-Controlled, Randomized Trial.” In:
Nutrition Research. 2008; 28: p. 1.
KATO-KATAOKA, A. ET al.: “Fermented Milk Containing Lactobacillus casei Strain Shirota
Preserves the Diversity of the Gut Microbiota and Relieves Abdominal Dysfunction in
Healthy Medical Students Exposed to Academic Stress.” In: Appl Environ Microbiol.
2016; 82: pp. 3649–3658.
KELLY, J.R. ET al.: “Transferring the Blues: Depression-Associated Gut Microbiota Induces
Neurobehavioural Changes in the Rat.” In: Psychiatr. Res. 2016; 82: pp. 109–118.
KRUIJT, A.W. ET al.: “Cognitive Reactivity, Implicit Associations, and the Incidence of
Depression: a Two-Year Prospective Study.” In: PLoS One. 2013; 8 (7), e70245.
MCKEAN, J. ET al.: “Probiotics and Subclinical Psychological Symptoms in Healthy
Participants: A Systematic Review and Meta-Analysis.” In: J. Altern Complement Med.
2017 April; 23 (4): pp. 249–258. doi: 10.1089/acm.2016.0023. Epub 2016 November 14.
MESSAOUDI, M. ET al.: “Beneficial Psychological Effects of a Probiotic Formulation
(Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in Healthy Human
Volunteers.” In: Gut Microbes. 2011 July-August; 2 (4): pp. 256–261. doi:
10.4161/gmic.2.4.16108. Epub 2011 July 1.
ROMIJN, A.R. ET al.: “Double-Blind, Randomized, Placebo-Controlled Trial of Lactobacillus
helveticus and Bifidobacterium longum for the Symptoms of Depression.” In: Australian
& New Zealand Journal of Psychiatry. 2017 August; 51 (8): pp. 810–821. doi:
10.1177/0004867416686694. Epub 2017 January 10.
SARKAR, A. ET al.: “Psychobiotics and the Manipulation of Bacteria-Gut-Brain Signals.” In:
Trends Neurosci. 2016 November; 39 (11): pp. 763–781.
STEENBERGEN, L. ET al.: “A Randomized Controlled Trial to Test the Effect of
Multispecies Probiotics on Cognitive Reactivity to Sad Mood.” In: Brain, Behavior, and
Immunity. 2015 August; 48: pp. 258–264.
About the Author
GIULIA ENDERS, MD, is a resident doctor for Internal Medicine and
Gastroenterology and a two-time scholarship winner of the Wilhelm
and Else Heraeus Foundation. She lives in Mannheim and Frankfurt,
Germany.
About the Illustrator
JILL ENDERS is a graphic designer whose main focus is
communication in science. She received a scholarship from the
Heinrich Hertz Society for her work. In 2013, she founded a
collaborative network of designers and scientists.
Copyright © 2015, 2018 by Giulia Enders
Illustrations copyright © 2015, 2018 by Jill Enders
Translation copyright © 2015, 2018 by David Shaw
Originally published in Germany as Darm mit Charme by Ullstein 2014
First published in English by Scribe 2015
All rights reserved. No part of this book may be reproduced, stored in a retrieval system or
transmitted, in any form or by any means, without the prior written consent of the publisher
or a license from The Canadian
Copyright Licensing Agency (Access Copyright). For a copyright license, visit
www.accesscopyright.ca or call toll free to 1-800-893-5777.
Greystone Books Ltd.
greystonebooks.com
Cataloguing data available from Library and Archives Canada
ISBN 978-1-77164-376-4 pbk.
ISBN 978-1-77164-378-8 epub
Editing by Jane Billinghurst
Cover and interior illustrations by Jill Enders
Cover and interior design by Peter Cocking and Nayeli Jimenez
We gratefully acknowledge the support of the Canada Council for the Arts, the British
Columbia Arts Council, the Province of British Columbia through the Book Publishing Tax
Credit, and the Government of Canada for our publishing activities.
The advice provided in this book has been carefully considered and checked by the author
and publisher. It should not, however, be regarded as a substitute for competent medical
advice. Therefore, all information in this book is provided without any warranty or guarantee
on the part of the publisher or the author. Neither the author nor the publisher or their
representatives shall bear any
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